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        <title>Endocrinology via MedWorm.com</title>
        <description>MedWorm.com provides a medical RSS filtering service. Over 6000 RSS medical sources are combined and output via different filters. This feed contains the latest items from the 'Endocrinology' source.</description>
        <link><![CDATA[http://www.medworm.com/rss/search.php?qu=Endocrinology&t=Endocrinology&s=Search&f=source]]></link>
        <lastBuildDate>Sun, 21 Mar 2010 15:01:33 +0100</lastBuildDate>
        <item>
            <title>Regulation of the Matricellular Proteins CYR61 (CCN1) and NOV (CCN3) by Hypoxia-Inducible Factor-1{alpha} and Transforming-Growth Factor-{beta}3 in the Human Trophoblast.</title>
            <link>http://www.medworm.com/index.php?rid=3383537&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20237132%26dopt%3DAbstract</link>
            <description>Authors: Wolf N, Yang W, Dunk CE, Gashaw I, Lye SJ, Ring T, Schmidt M, Winterhager E, Gellhaus A
    It is known that a hypoxic environment is critical for trophoblast migration and invasion and is fundamental for appropriate placental perfusion. Because cysteine-rich 61 (CYR61, CCN1) and nephroblastoma overexpressed (NOV, CCN3) are expressed in the extravillous trophoblast and expression levels are deregulated in preeclampsia, we investigated their regulation properties in first-trimester placental explants and in JEG3 choriocarcinoma cells upon a physiological low oxygen tension of 1-3%. In placental explants, both proteins were expressed in the extravillous trophoblast cells and were increased upon hypoxia. JEG3 cells revealed a significant up-regulation of CYR61 and NOV intracellular a...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3383537</comments>
            <pubDate>Wed, 17 Mar 2010 00:00:00 +0100</pubDate>
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            <title>Sex Differences in Epigenetic Regulation of the Estrogen Receptor-{alpha} Promoter within the Developing Preoptic Area.</title>
            <link>http://www.medworm.com/index.php?rid=3383536&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20237133%26dopt%3DAbstract</link>
            <description>Authors: Kurian JR, Olesen KM, Auger AP
    Sex differences in the brain are largely organized by a testicular hormone surge that occurs in males shortly after birth. Although this hormone surge is transient, sex differences in brain and behavior are lasting. Here we describe a sex difference in DNA methylation of the estrogen receptor-alpha (ERalpha) promoter region within the developing rat preoptic area, with males exhibiting more DNA methylation within the ERalpha promoter than females. More importantly, we report that simulating maternal grooming, a form of maternal interaction that is sexually dimorphic with males experiencing more than females during the neonatal period, effectively masculinizes female ERalpha promoter methylation and gene expression. This suggests natural variation...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3383536</comments>
            <pubDate>Wed, 17 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3383536</guid>        </item>
        <item>
            <title>A Mouse Model of Androgenetic Alopecia.</title>
            <link>http://www.medworm.com/index.php?rid=3383542&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20233794%26dopt%3DAbstract</link>
            <description>Authors: Crabtree JS, Kilbourne EJ, Peano BJ, Chippari S, Kenney T, McNally C, Wang W, Harris HA, Winneker RC, Nagpal S, Thompson CC
    Androgenetic alopecia (AGA), commonly known as male pattern baldness, is a form of hair loss that occurs in both males and females. Although the exact cause of AGA is not known, it is associated with genetic predisposition through traits related to androgen synthesis/metabolism and androgen signaling mediated by the androgen receptor (AR). Current therapies for AGA show limited efficacy and are often associated with undesirable side effects. A major hurdle to developing new therapies for AGA is the lack of small animal models to support drug discovery research. Here, we report the first rodent model of AGA. Previous work demonstrating that the interaction...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3383542</comments>
            <pubDate>Tue, 16 Mar 2010 00:00:00 +0100</pubDate>
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        <item>
            <title>Functional Roles of Protein Kinase A (PKA) and Exchange Protein Directly Activated by 3',5'-Cyclic Adenosine 5'-Monophosphate (cAMP) 2 (EPAC2) in cAMP-Mediated Actions in Adrenocortical Cells.</title>
            <link>http://www.medworm.com/index.php?rid=3383541&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20233795%26dopt%3DAbstract</link>
            <description>Authors: Aumo L, Rusten M, Mellgren G, Bakke M, Lewis AE
    In the adrenal cortex, the biosynthesis of steroid hormones is controlled by the pituitary-derived hormone ACTH. The functions of ACTH are principally relayed by activating cAMP-dependent signaling pathways leading to the induction of genes encoding enzymes involved in the conversion of cholesterol to steroid hormones. Previously, protein kinase A (PKA) was thought to be the only direct effector of cAMP. However, the discovery of the cAMP sensors, exchange proteins directly activated by cAMP (EPAC1 and 2), has led to a reevaluation of this assumption. In the present study, we demonstrate the occurrence of the EPAC2 splicing variant EPAC2B in adrenocortical cancer cells. Immunocytochemistry demonstrated that EPAC2B is localized pr...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3383541</comments>
            <pubDate>Tue, 16 Mar 2010 00:00:00 +0100</pubDate>
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        <item>
            <title>In Vivo Molecular Imaging of Somatostatin Receptors in Pancreatic Islet Cells and Neuroendocrine Tumors by Miniaturized Confocal Laser-Scanning Fluorescence Microscopy.</title>
            <link>http://www.medworm.com/index.php?rid=3383540&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20233796%26dopt%3DAbstract</link>
            <description>Authors: Fottner C, Mettler E, Goetz M, Schirrmacher E, Anlauf M, Strand D, Schirrmacher R, Kl&amp;#xF6;ppel G, Delaney P, Schreckenberger M, Galle PR, Neurath MF, Kiesslich R, Weber MM
    The aim of the study was to evaluate real time in vivo molecular imaging of somatostatin receptors (sstrs) using a handheld miniaturized confocal laser scan microscope (CLM) in conjunction with fluorescein-labeled octreotate (OcF) in healthy mice and murine models of neuroendocrine tumors. For CLM a small rigid probe (diameter 7 mm) with an integrated single line laser (488 nm) was used (optical slice thickness 7 mum; lateral resolution 0.7 mum). OcF was synthesized via Fmoc solid-phase peptide synthesis and purified by HPLC showing high-affinity binding to the sstr2 (IC50 6.2 nmol). For in vitro evaluation...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3383540</comments>
            <pubDate>Tue, 16 Mar 2010 00:00:00 +0100</pubDate>
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        <item>
            <title>Overlapping Roles of the Glucose-Responsive Genes, S14 and S14R, in Hepatic Lipogenesis.</title>
            <link>http://www.medworm.com/index.php?rid=3383539&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20233797%26dopt%3DAbstract</link>
            <description>Authors: Aipoalani DL, O'Callaghan BL, Mashek DG, Mariash CN, Towle HC
    The Spot 14 (S14; Thrsp) gene has been implicated in supporting regulated lipogenesis in mammals. S14 gene expression in liver is controlled by a wide variety of hormones and dietary factors in parallel with the major lipogenic enzyme genes. In addition, mice deleted for the S14 gene display reduced de novo lipogenesis in the lactating mammary gland. However, no decrease in hepatic lipogenesis was observed in the S14 null mouse. It was postulated that this difference could be due to the expression of a paralogous gene called S14R (S14 related; Mig12) in the liver but not mammary tissue. To test this hypothesis, we used small interfering RNA to simultaneously reduce levels of S14 and S14R in cultured primary hepatocy...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3383539</comments>
            <pubDate>Tue, 16 Mar 2010 00:00:00 +0100</pubDate>
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        <item>
            <title>The Ontogeny of Insulin Signaling in the Preterm Baboon Model.</title>
            <link>http://www.medworm.com/index.php?rid=3383538&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20233798%26dopt%3DAbstract</link>
            <description>In conclusion, significant gestational differences exist in the protein content of several insulin signaling proteins in the muscle of fetal baboons. Reduced muscle content of key glucose transport-regulating proteins (GLUT1, GLUT4, AS160) could play a role in the pathogenesis of neonatal hyperglycemia and reduced insulin-stimulated glucose disposal.
    PMID: 20233798 [PubMed - as supplied by publisher] (Source: Endocrinology)</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3383538</comments>
            <pubDate>Tue, 16 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3383538</guid>        </item>
        <item>
            <title>CCAAT/Enhancer Binding Protein {beta}2 Is Involved in Growth Hormone-Regulated Insulin-Like Growth Factor-II Gene Expression in the Liver of Rainbow Trout (Oncorhynchus mykiss).</title>
            <link>http://www.medworm.com/index.php?rid=3374963&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20228168%26dopt%3DAbstract</link>
            <description>Authors: Lo JH, Chen TT
    Previously, we showed that levels of different CCAAT/enhancer binding protein (C/EBP) mRNAs in the liver of rainbow trout were modulated by GH and suggested that C/EBPs might be involved in GH-induced IGF-II gene expression. As a step toward further investigation, we have developed monospecific polyclonal antibodies to detect rainbow trout C/EBPalpha, -beta1, -beta2, and -delta2 isoform proteins. Injection of GH into adult rainbow trout resulted in a significant increase of C/EBPbeta1, C/EBPbeta2, and C/EBPdelta2 proteins in the liver. Chromatin immunoprecipitation analysis revealed that C/EBPbeta2 binds to multiple sites at the 5' promoter/regulatory region, introns, and the 3' untranslated region of the IGF-II gene. GH treatment reduced C/EBPbeta2 binding to s...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3374963</comments>
            <pubDate>Fri, 12 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3374963</guid>        </item>
        <item>
            <title>Long-Term Ritonavir Exposure Increases Fatty Acid and Glycerol Recycling in 3T3-L1 Adipocytes as Compensatory Mechanisms for Increased Triacylglycerol Hydrolysis.</title>
            <link>http://www.medworm.com/index.php?rid=3374962&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20228169%26dopt%3DAbstract</link>
            <description>Authors: Adler-Wailes DC, Guiney EL, Wolins NE, Yanovski JA
    Lipodystrophy with high nonesterified fatty acid (FA) efflux is reported in humans receiving highly active antiretroviral therapy (HAART) to treat HIV infection. Ritonavir, a common component of HAART, alters adipocyte FA efflux, but the mechanism for this effect is not established. To investigate ritonavir-induced changes in FA flux and recycling through acylglycerols, we exposed differentiated murine 3T3-L1 adipocytes to ritonavir for 14 d. FA efflux, uptake, and incorporation into acylglycerols were measured. To identify a mediator of FA efflux, we measured adipocyte triacylglycerol lipase (ATGL) transcript and protein. To determine whether ritonavir-treated adipocytes increased glycerol backbone synthesis for FA reesterifi...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3374962</comments>
            <pubDate>Fri, 12 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3374962</guid>        </item>
        <item>
            <title>Direct Action through the Sertoli Cells Is Essential for Androgen Stimulation of Spermatogenesis.</title>
            <link>http://www.medworm.com/index.php?rid=3374961&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20228170%26dopt%3DAbstract</link>
            <description>Authors: O'Shaughnessy PJ, Verhoeven G, De Gendt K, Monteiro A, Abel MH
    Androgens act to stimulate spermatogenesis through androgen receptors (ARs) on the Sertoli cells and peritubular myoid cells. Specific ablation of the AR in either cell type will cause a severe disruption of spermatogenesis. To determine whether androgens can stimulate spermatogenesis through direct action on the peritubular myoid cells alone or whether action on the Sertoli cells is essential, we crossed hypogonadal (hpg) mice that lack gonadotrophins and intratesticular androgen with mice lacking ARs either ubiquitously (ARKO) or specifically on the Sertoli cells (SCARKO). These hpg.ARKO and hpg.SCARKO mice were treated with testosterone (T) or dihydrotestosterone (DHT) for 7 d and testicular morphology and cell ...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3374961</comments>
            <pubDate>Fri, 12 Mar 2010 00:00:00 +0100</pubDate>
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        <item>
            <title>Oxytocin-Dopamine Interactions Mediate Variations in Maternal Behavior in the Rat.</title>
            <link>http://www.medworm.com/index.php?rid=3374960&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20228171%26dopt%3DAbstract</link>
            <description>Authors: Shahrokh DK, Zhang TY, Diorio J, Gratton A, Meaney MJ
    Variations in maternal behavior among lactating rats associate with differences in estrogen-oxytocin interactions in the medial preoptic area (mPOA) and in dopamine levels in the nucleus accumbens (nAcc). Thus, stable, individual differences in pup licking/grooming (LG) are abolished by oxytocin receptor blockade or treatments that eliminate differences in the nAcc dopamine signal. We provide novel evidence for a direct effect of oxytocin at the level of the ventral tegmental area (VTA) in the regulation of nAcc dopamine levels. Mothers that exhibit consistently increased pup LG (i.e. high LG mothers) by comparison with low LG mothers show increased oxytocin expression in the mPOA and the paraventricular nucleus of the hypo...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3374960</comments>
            <pubDate>Fri, 12 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3374960</guid>        </item>
        <item>
            <title>Adaptations of the Autonomous Nervous System Controlling Heart Rate Are Impaired by a Mutant Thyroid Hormone Receptor-{alpha}1.</title>
            <link>http://www.medworm.com/index.php?rid=3374959&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20228172%26dopt%3DAbstract</link>
            <description>Authors: Mittag J, Davis B, Vujovic M, Arner A, Vennstr&amp;#xF6;m B
    Thyroid hormone has profound direct effects on cardiac function, but the hormonal interactions with the autonomic control of heart rate are unclear. Because thyroid hormone receptor (TR)-alpha1 has been implicated in the autonomic control of brown adipose energy metabolism, it might also play an important role in the central autonomic control of heart rate. Thus, we aimed to analyze the role of TRalpha1 signaling in the autonomic control of heart rate using an implantable radio telemetry system. We identified that mice expressing the mutant TRalpha1R384C (TRalpha1+m mice) displayed a mild bradycardia, which becomes more pronounced during night activity or on stress and is accompanied by a reduced expression of nucleotide-...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3374959</comments>
            <pubDate>Fri, 12 Mar 2010 00:00:00 +0100</pubDate>
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        <item>
            <title>Chemerin Exacerbates Glucose Intolerance in Mouse Models of Obesity and Diabetes.</title>
            <link>http://www.medworm.com/index.php?rid=3374958&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20228173%26dopt%3DAbstract</link>
            <description>Authors: Ernst MC, Issa M, Goralski KB, Sinal CJ
    Obesity, characterized by an excess of adipose tissue, is an established risk factor for cardiovascular disease and type 2 diabetes. Different mechanisms linking obesity with these comorbidities have been postulated but remain poorly understood. Adipose tissue secretes a number of hormone-like compounds, termed adipokines, that are important for the maintenance of normal glucose metabolism. Alterations in the secretion of adipokines with obesity are believed to contribute to the undesirable changes in glucose metabolism that ultimately result in the development of type 2 diabetes. In the present study, we have shown that serum levels of the novel adipokine chemerin are significantly elevated in mouse models of obesity/diabetes. The expre...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3374958</comments>
            <pubDate>Fri, 12 Mar 2010 00:00:00 +0100</pubDate>
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        <item>
            <title>Thyroid Hormone-Regulated Mouse Cerebral Cortex Genes Are Differentially Dependent on the Source of the Hormone: A Study in Monocarboxylate Transporter-8- and Deiodinase-2-Deficient Mice.</title>
            <link>http://www.medworm.com/index.php?rid=3357607&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20211971%26dopt%3DAbstract</link>
            <description>Authors: Morte B, Ceballos A, Diez D, Grijota-Mart&amp;#xED;nez C, Dumitrescu AM, Di Cosmo C, Galton VA, Refetoff S, Bernal J
    Thyroid hormones influence brain development through the control of gene expression. The concentration of the active hormone T3 in the brain depends on T3 transport through the blood-brain barrier, mediated in part by the monocarboxylate transporter 8 (Mct8/MCT8) and the activity of type 2 deiodinase (D2) generating T3 from T4. The relative roles of each of these pathways in the regulation of brain gene expression is not known. To shed light on this question, we analyzed thyroid hormone-dependent gene expression in the cerebral cortex of mice with inactivated Mct8 (Slc16a2) and Dio2 genes, alone or in combination. We used 34 target genes identified to be controlled ...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3357607</comments>
            <pubDate>Wed, 10 Mar 2010 00:00:00 +0100</pubDate>
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        <item>
            <title>The Positive Effects of Growth Hormone-Releasing Peptide-6 on Weight Gain and Fat Mass Accrual Depend on the Insulin/Glucose Status.</title>
            <link>http://www.medworm.com/index.php?rid=3357594&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20219977%26dopt%3DAbstract</link>
            <description>In conclusion, GHRP-6 and insulin exert an additive effect on weight gain and visceral fat mass accrual in diabetic rats, indicating that some of GHRP-6's metabolic effects depend on the insulin/glucose status.
    PMID: 20219977 [PubMed - as supplied by publisher] (Source: Endocrinology)</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3357594</comments>
            <pubDate>Wed, 10 Mar 2010 00:00:00 +0100</pubDate>
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            <title>Expression of E-Cadherin and N-Cadherin in Perinatal Hamster Ovary: Possible Involvement in Primordial Follicle Formation and Regulation by Follicle-Stimulating Hormone.</title>
            <link>http://www.medworm.com/index.php?rid=3357593&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20219978%26dopt%3DAbstract</link>
            <description>We examined the expression and hormonal regulation of E-cadherin (CDH1) and N-cadherin (CDH2) with respect to primordial follicle formation. Hamster Cdh1 and Cdh2 cDNA and amino acid sequences were more than 90% similar to those of the mouse, rat, and human. Although CDH1 expression remained exclusively in the oocytes during neonatal ovary development, CDH2 expression shifted from the oocytes to granulosa cells of primordial follicles on postnatal day (P)8. Subsequently, strong CDH2 expression was restricted to granulosa cells of growing follicles. Cdh2 mRNA levels in the ovary decreased from embryonic d 13 through P10 with a transient increase on P7, which was the day before the appearance of primordial follicles. Cdh1 mRNA levels decreased from embryonic d 13 through P3 and then showed a...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3357593</comments>
            <pubDate>Wed, 10 Mar 2010 00:00:00 +0100</pubDate>
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        <item>
            <title>Glioma Pathogenesis-Related 1-Like 1 Is Testis Enriched, Dynamically Modified, and Redistributed during Male Germ Cell Maturation and Has a Potential Role in Sperm-Oocyte Binding.</title>
            <link>http://www.medworm.com/index.php?rid=3357591&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20219979%26dopt%3DAbstract</link>
            <description>Authors: Gibbs GM, Lo JC, Nixon B, Jamsai D, O'Connor AE, Rijal S, Sanchez-Partida LG, Hearn MT, Bianco DM, O'Bryan MK
    The glioma pathogenesis-related 1 (GLIPR1) family consists of three genes [GLIPR1, GLIPR1-like 1 (GLIPR1L1), and GLIPR1-like 2 (GLIPR1L2)] and forms a distinct subgroup within the cysteine-rich secretory protein (CRISP), antigen 5, and pathogenesis-related 1 (CAP) superfamily. CAP superfamily proteins are found in phyla ranging from plants to humans and, based largely on expression and limited functional studies, are hypothesized to have roles in carcinogenesis, immunity, cell adhesion, and male fertility. Specifically data from a number of systems suggests that sequences within the C-terminal CAP domain of CAP proteins have the ability to promote cell-cell adhesion. H...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3357591</comments>
            <pubDate>Wed, 10 Mar 2010 00:00:00 +0100</pubDate>
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        <item>
            <title>Prolactin Increases the Synthesis of 7{alpha}-Hydroxypregnenolone, a Key Factor for Induction of Locomotor Activity, in Breeding Male Newts.</title>
            <link>http://www.medworm.com/index.php?rid=3357587&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20219980%26dopt%3DAbstract</link>
            <description>In this study, cytochrome P4507alpha (CYP7B), a steroidogenic enzyme catalyzing the formation of 7alpha-hydroxypregnenolone, was first identified to analyze seasonal changes in 7alpha-hydroxypregnenolone synthesis. Only males exhibited marked seasonal changes in 7alpha-hydroxypregnenolone synthesis and CYP7B expression in the brain, with a maximum level in the spring breeding period when locomotor activity of males increases. Subsequently we identified PRL as a key component of the mechanism regulating 7alpha-hydroxypregnenolone synthesis. Hypophysectomy decreased 7alpha-hydroxypregnenolone synthesis in the male brain, whereas administration of PRL but not gonadotropins to hypophysectomized males caused a dose-dependent increase in 7alpha-hydroxypregnenolone synthesis. To analyze the mode ...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3357587</comments>
            <pubDate>Wed, 10 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3357587</guid>        </item>
        <item>
            <title>Exendin-4 Prevents c-Jun N-Terminal Protein Kinase Activation by Tumor Necrosis Factor-{alpha} (TNF{alpha}) and Inhibits TNF{alpha}-Induced Apoptosis in Insulin-Secreting Cells.</title>
            <link>http://www.medworm.com/index.php?rid=3357586&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20219981%26dopt%3DAbstract</link>
            <description>In conclusion, JNK activation mediates TNFalpha-induced apoptosis and impairment of the IRS/Akt signaling pathway in insulin-secreting cells. By inhibiting JNK phosphorylation in a PKA-dependent manner, exendin-4 counteracts TNFalpha-mediated apoptosis and reverses the inhibitory events in the IRS/Akt pathway, resulting in promotion of cell survival.
    PMID: 20219981 [PubMed - as supplied by publisher] (Source: Endocrinology)</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3357586</comments>
            <pubDate>Wed, 10 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3357586</guid>        </item>
        <item>
            <title>Phospholipase D2 Mediates Acute Aldosterone Secretion in Response to Angiotensin II in Adrenal Glomerulosa Cells.</title>
            <link>http://www.medworm.com/index.php?rid=3357585&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20219982%26dopt%3DAbstract</link>
            <description>Authors: Qin H, Frohman MA, Bollag WB
    In primary bovine adrenal glomerulosa cells, the signaling enzyme phospholipase D (PLD) is suggested to mediate priming, the enhancement of aldosterone secretion after pretreatment with and removal of angiotensin II (AngII), via the formation of persistently elevated diacylglycerol (DAG). To further explore PLD's role in priming, glomerulosa cells were pretreated with an exogenous bacterial PLD. Using this approach, phosphatidic acid (PA) is generated on the outer, rather than the inner, leaflet of the plasma membrane. Although PA is not readily internalized, the PA is nonetheless rapidly hydrolyzed by cell-surface PA phosphatases to DAG, which efficiently flips to the inner leaflet and accesses the cell interior. Pretreatment with bacterial PLD re...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3357585</comments>
            <pubDate>Wed, 10 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3357585</guid>        </item>
        <item>
            <title>The Highly Conserved Gonadotropin-Releasing Hormone-2 Form Acts as a Melatonin-Releasing Factor in the Pineal of a Teleost Fish, the European Sea Bass Dicentrarchus labrax.</title>
            <link>http://www.medworm.com/index.php?rid=3357599&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20215565%26dopt%3DAbstract</link>
            <description>In this study performed on a perciform fish, the European sea bass, we show for the first time that the pineal organ receives GnRH-2-immunoreactive fibers originating from the synencephalic GnRH-2 neurons. This was shown through a combination of retrograde tracing and immunohistochemistry, using highly specific antibodies. Supporting the presence of GnRH-2 functional targets, RT-PCR data together with the in situ hybridization studies showed that the sea bass pineal gland strongly expressed a GnRH receptor (dlGnRHR-II-2b) with clear selectivity for GnRH-2 and, to a lesser extent, the dlGnRHR-II-1a subtype. Finally, in vitro and in vivo experiments demonstrate stimulatory effects of GnRH-2 on nocturnal melatonin secretion by the sea bass pineal organ. Altogether, these data provide, for the...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3357599</comments>
            <pubDate>Tue, 09 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3357599</guid>        </item>
        <item>
            <title>Activity of Retinoic Acid Receptor-{alpha} Is Directly Regulated at Its Protein Kinase A Sites in Response to Follicle-Stimulating Hormone Signaling.</title>
            <link>http://www.medworm.com/index.php?rid=3357598&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20215566%26dopt%3DAbstract</link>
            <description>Authors: Santos NC, Kim KH
    Retinoic acid receptor-alpha (RARA) is crucial for germ cell development in the testis, as shown by the degenerated testis in Rara gene knockout mice, which are sterile. Similarly, FSH is known to regulate Sertoli cell proliferation and differentiation, indirectly controlling the quantity of the spermatogenic output. Interestingly, FSH inhibited, via activation of FSH receptor, cAMP, and protein kinase A (PKA), the nuclear localization and transcriptional activity of RARA. Given that retinoic acid, the ligand for RARA, is known to regulate cell proliferation and differentiation, we investigated whether FSH regulates RARA by a direct posttranslational phosphorylation mechanism. Mutagenesis of serine 219 (S219) and S369 at the PKA sites on RARA to either double...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3357598</comments>
            <pubDate>Tue, 09 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3357598</guid>        </item>
        <item>
            <title>Episodes of Prolactin Gene Expression in GH3 Cells Are Dependent on Selective Promoter Binding of Multiple Circadian Elements.</title>
            <link>http://www.medworm.com/index.php?rid=3357597&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20215567%26dopt%3DAbstract</link>
            <description>In this study, we used serum-shocked GH3 cells, established previously to synchronize PRL pulses between cells in culture, to reveal that pulses of PRL mRNA are linked temporally to the expression of bmal1, cry1, per1, and per3 mRNA in these cells. Moreover, we found that each of these circadian factors binds to the rat PRL promoter by chromatin immunoprecipitation analysis. Using EMSA analysis, we observed that two sites present in the proximal promoter region, E-box133 and E-box10, bind circadian factors differentially (E-box133 interacted with BMAL1, cryptochrome-1, period (PER)-1, and PER3 but not PER2 and E-box10 bound BMAL1, cryptochrome-1, PER2, PER3 but not PER1). More importantly, down-regulation of any factor binding E-box133 significantly reduced PRL mRNA levels during pulse per...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3357597</comments>
            <pubDate>Tue, 09 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3357597</guid>        </item>
        <item>
            <title>Insulinoma-Associated Antigen-1 Zinc-Finger Transcription Factor Promotes Pancreatic Duct Cell Trans-Differentiation.</title>
            <link>http://www.medworm.com/index.php?rid=3357596&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20215568%26dopt%3DAbstract</link>
            <description>Authors: Zhang T, Wang H, Saunee NA, Breslin MB, Lan MS
    Insulinoma-associated antigen-1 (INSM1/IA-1) is a unique zinc-finger transcription factor restrictedly expressed in pancreatic beta-cells during early pancreas development. INSM1 is transiently activated by the islet-specific endocrine factor neurogenin 3, and it subsequently regulates downstream target genes NeuroD1 and insulin during beta-cell maturation. Here, we examined how the INSM1 transcription factor contributes to endocrine cell differentiation using a defined serum-free medium-primed pancreatic duct cell model. We showed that ectopic expression of INSM1 can promote Panc-1 cell trans-differentiation. INSM1 up-regulates two islet transcription factors (ITFs), paired box 6 and homeodomain transcription factor 6.1, whereas ...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3357596</comments>
            <pubDate>Tue, 09 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3357596</guid>        </item>
        <item>
            <title>Glucose Intolerance and Impaired Insulin Secretion in Pancreas-Specific Signal Transducer and Activator of Transcription-3 Knockout Mice Are Associated with Microvascular Alterations in the Pancreas.</title>
            <link>http://www.medworm.com/index.php?rid=3357595&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20215569%26dopt%3DAbstract</link>
            <description>Authors: Kostromina E, Gustavsson N, Wang X, Lim CY, Radda GK, Li C, Han W
    Maintenance of glucose homeostasis depends on adequate amount and precise pattern of insulin secretion, which is determined by both beta-cell secretory processes and well-developed microvascular network within endocrine pancreas. The development of highly organized microvasculature and high degrees of capillary fenestrations in endocrine pancreas is greatly dependent on vascular endothelial growth factor-A (VEGF-A) from islet cells. However, it is unclear how VEGF-A production is regulated in endocrine pancreas. To understand whether signal transducer and activator of transcription (STAT)-3 is involved in VEGF-A regulation and subsequent islet and microvascular network development, we generated a mouse line carr...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3357595</comments>
            <pubDate>Tue, 09 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3357595</guid>        </item>
        <item>
            <title>Electrical and Morphological Characteristics of Anteroventral Periventricular Nucleus Kisspeptin and Other Neurons in the Female Mouse.</title>
            <link>http://www.medworm.com/index.php?rid=3357610&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20211970%26dopt%3DAbstract</link>
            <description>Authors: Ducret E, Gaidamaka G, Herbison AE
    Neurons in the rodent anteroventral periventricular nucleus (AVPV) play a key role in integrating circadian and gonadal steroid hormone information in the control of fertility. In particular, estradiol-sensitive kisspeptin neurons located in the AVPV, and adjacent structures [together termed the rostral periventricular area of the third ventricle (RP3V)], are critical for puberty onset and the preovulatory LH surge. The present study aimed to establish the morphological and electrical firing characteristics of RP3V neurons, including kisspeptin neurons, in the adult female mouse. Cell-attached electrical recordings, followed by juxtacellular dye filling, of 129 RP3V neurons in the acute brain slice preparation revealed these cells to exhibit ...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3357610</comments>
            <pubDate>Mon, 08 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3357610</guid>        </item>
        <item>
            <title>Endocrine and Physiological Changes in Response to Chronic Corticosterone: A Potential Model of the Metabolic Syndrome in Mouse.</title>
            <link>http://www.medworm.com/index.php?rid=3357606&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20211972%26dopt%3DAbstract</link>
            <description>Authors: Karatsoreos IN, Bhagat SM, Bowles NP, Weil ZM, Pfaff DW, McEwen BS
    Numerous clinical and experimental studies have linked stress to changes in risk factors associated with the development of physiological syndromes, including metabolic disorders. How different mediators of the stress response, such as corticosterone (CORT), influence these changes in risk remains unclear. Although CORT has beneficial short-term effects, long-term CORT exposure can result in damage to the physiological systems it protects acutely. Disruption of this important physiologic signal is observed in numerous disparate disorders, ranging from depression to Cushing's syndrome. Thus, understanding the effects of chronic high CORT on metabolism and physiology is of key importance. We explored the effects ...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3357606</comments>
            <pubDate>Mon, 08 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3357606</guid>        </item>
        <item>
            <title>Spironolactone Improves Glucose and Lipid Metabolism by Ameliorating Hepatic Steatosis and Inflammation and Suppressing Enhanced Gluconeogenesis Induced by High-Fat and High-Fructose Diet.</title>
            <link>http://www.medworm.com/index.php?rid=3357600&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20211973%26dopt%3DAbstract</link>
            <description>Authors: Wada T, Kenmochi H, Miyashita Y, Sasaki M, Ojima M, Sasahara M, Koya D, Tsuneki H, Sasaoka T
    Recent evidence suggests that treatment with mineralocorticoid receptor antagonist suppressed local inflammation in vascular tissues or cardiomyocytes; therefore, we examined the effect of spironolactone on glucose and lipid metabolism in a mouse model with diet-induced diabetes and nonalcoholic fatty liver disease. C57BL/6 mice were fed either the control diet, 60% fat diet with 30% fructose water (HFFD), or HFFD with spironolactone for 8 wk. HFFD mice demonstrated apparent phenotypes of metabolic syndrome, including insulin resistance, hypertension, dyslipidemia, and fatty liver. Although treatment with spironolactone did not affect the increased calorie intake and body weight by HFF...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3357600</comments>
            <pubDate>Mon, 08 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3357600</guid>        </item>
        <item>
            <title>A Maternal &quot;Junk Food&quot; Diet in Pregnancy and Lactation Promotes Nonalcoholic Fatty Liver Disease in Rat Offspring.</title>
            <link>http://www.medworm.com/index.php?rid=3357625&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20207831%26dopt%3DAbstract</link>
            <description>This study examines whether a maternal junk food diet predisposes offspring to nonalcoholic fatty liver disease. The 144 rat offspring were fed either a balanced chow diet alone or with palatable junk foods rich in energy, fat, sugar, and/or salt during gestation, lactation, and/or after weaning up to the end of adolescence. Offspring fed junk food throughout the study exhibited exacerbated hepatic steatosis, hepatocyte ballooning, and oxidative stress response compared with offspring given free access to junk food after weaning only. These offspring also displayed sex differences in their hepatic molecular metabolic adaptation to diet-induced obesity with increased expression of genes associated with insulin sensitivity, de novo lipogenesis, lipid oxidation, and antiinflammatory propertie...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3357625</comments>
            <pubDate>Fri, 05 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3357625</guid>        </item>
        <item>
            <title>Kisspeptin Cells in the Ewe Brain Respond to Leptin and Communicate with Neuropeptide Y and Proopiomelanocortin Cells.</title>
            <link>http://www.medworm.com/index.php?rid=3357624&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20207832%26dopt%3DAbstract</link>
            <description>Authors: Backholer K, Smith JT, Rao A, Pereira A, Iqbal J, Ogawa S, Li Q, Clarke IJ
    Kisspeptin stimulates reproduction, and kisspeptin cells in the arcuate nucleus (ARC) express Ob-Rb in the mouse. Herein we report studies in ewes to determine whether kisspeptin cells express Ob-Rb and respond to leptin and whether reciprocal connections exist between kisspeptin cells and proopiomelanocortin (POMC) or neuropeptide Y (NPY) cells to modulate reproduction and metabolic function. Kiss1 mRNA was measured by in situ hybridization in ovariectomized ewes that were normal body weight, lean, or lean with leptin treatment by intracerebroventricular (icv) infusion (4 mug/h, 3 d). Kiss1 expression in the ARC and the preoptic area was lower in hypogonadotropic lean animals than animals of normal wei...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3357624</comments>
            <pubDate>Fri, 05 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3357624</guid>        </item>
        <item>
            <title>Hypothalamic Kiss1 but Not Kiss2 Neurons Are Involved in Estrogen Feedback in Medaka (Oryzias latipes).</title>
            <link>http://www.medworm.com/index.php?rid=3357619&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20207833%26dopt%3DAbstract</link>
            <description>Authors: Mitani Y, Kanda S, Akazome Y, Zempo B, Oka Y
    Kiss2, a paralogous gene for kiss1, has recently been identified in several vertebrates. However, their relative potencies for the regulation of reproductive functions appear to differ among species. Here we used medaka as a model animal to examine the kiss1 and kiss2 expression dynamics by in situ hybridization under different conditions: breeding or nonbreeding and ovariectomized or sham operated. Medaka kiss1-expressing neurons and kiss2-expressing neurons were mainly localized in two hypothalamic nuclei, nucleus ventralis tuberis (NVT) and nucleus recessus lateralis (NRL), respectively. NRL kiss2 expression did not change according to differences in breeding condition, whereas NVT kiss1 expression was strongly correlated with br...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3357619</comments>
            <pubDate>Fri, 05 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3357619</guid>        </item>
        <item>
            <title>Regulation of Mineralocorticoid Receptor Expression during Neuronal Differentiation of Murine Embryonic Stem Cells.</title>
            <link>http://www.medworm.com/index.php?rid=3357613&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20207834%26dopt%3DAbstract</link>
            <description>In conclusion, we provide evidence for a tight transcriptional control of MR expression during neuronal differentiation. Given the neuroprotective and antiapoptotic role proposed for MR, the neuronal differentiation of ES cell lines opens potential therapeutic perspectives in neurological and psychiatric diseases.
    PMID: 20207834 [PubMed - as supplied by publisher] (Source: Endocrinology)</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3357613</comments>
            <pubDate>Fri, 05 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3357613</guid>        </item>
        <item>
            <title>Reduced Activity and Expression of Mitochondrial Citrate Carrier in Streptozotocin-Induced Diabetic Rats.</title>
            <link>http://www.medworm.com/index.php?rid=3338784&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20203153%26dopt%3DAbstract</link>
            <description>Authors: Gnoni GV, Giudetti AM, Mercuri E, Damiano F, Stanca E, Priore P, Siculella L
    Citrate carrier (CiC), an integral protein of the mitochondrial inner membrane, plays an important role in hepatic intermediary metabolism, supplying the cytosol with acetyl-coenzyme A for fatty acid and cholesterol synthesis. Here, the effect of streptozotocin-induced diabetes on CiC activity and expression in rat liver was investigated. The rate of citrate transport was reduced by about 35% in mitochondria from diabetic vs. control rats. Kinetic studies in mitochondria from diabetic rats showed a reduction in maximum velocity and almost unchanged Michaelis-Menten constant of the CiC protein. Mitochondrial phospholipid amount was not significantly affected, whereas an increase in the cholesterol cont...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3338784</comments>
            <pubDate>Thu, 04 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3338784</guid>        </item>
        <item>
            <title>Glucagon-Like Peptide-1 Receptor Agonists Activate Rodent Thyroid C-Cells Causing Calcitonin Release and C-Cell Proliferation.</title>
            <link>http://www.medworm.com/index.php?rid=3338783&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20203154%26dopt%3DAbstract</link>
            <description>Authors: Knudsen LB, Madsen LW, Andersen S, Almholt K, de Boer AS, Drucker DJ, Gotfredsen C, Egerod FL, Hegelund AC, Jacobsen H, Jacobsen SD, Moses AC, M&amp;#xF8;lck AM, Nielsen HS, Nowak J, Solberg H, Thi TD, Zdravkovic M
    Liraglutide is a glucagon-like peptide-1 (GLP-1) analog developed for type 2 diabetes. Long-term liraglutide exposure in rodents was associated with thyroid C-cell hyperplasia and tumors. Here, we report data supporting a GLP-1 receptor-mediated mechanism for these changes in rodents. The GLP-1 receptor was localized to rodent C-cells. GLP-1 receptor agonists stimulated calcitonin release, up-regulation of calcitonin gene expression, and subsequently C-cell hyperplasia in rats and, to a lesser extent, in mice. In contrast, humans and/or cynomolgus monkeys had low GLP-1 ...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3338783</comments>
            <pubDate>Thu, 04 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3338783</guid>        </item>
        <item>
            <title>The Lipoprivic Control of Feeding Is Governed by Fat Metabolism, Not by Leptin or Adipose Depletion.</title>
            <link>http://www.medworm.com/index.php?rid=3338782&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20203155%26dopt%3DAbstract</link>
            <description>Authors: Hudson BD, Emanuel AJ, Wiater MF, Ritter S
    A lipoprivic control of feeding has been proposed based on the finding that appetite is stimulated by drugs such as beta-mercaptoacetate (MA) that reduce fatty acid oxidation. The adipose-derived hormone, leptin, has effects on feeding and fat oxidation that are opposite those produced by MA. However, effects of this hormone on MA-induced feeding are not known. Here we examined the effects of endogenous leptin levels and of acute central and peripheral leptin administration on MA-induced feeding. We also examined leptin-induced changes in feeding, body weight, and plasma fuels after capsaicin-induced deletion of the lipoprivic control. MA-induced feeding was not altered under any of these conditions, and leptin's effects were not alte...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3338782</comments>
            <pubDate>Thu, 04 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3338782</guid>        </item>
        <item>
            <title>Androgen Receptor-Dependent Activation of Endothelial Nitric Oxide Synthase in Vascular Endothelial Cells: Role of Phosphatidylinositol 3-Kinase/Akt Pathway.</title>
            <link>http://www.medworm.com/index.php?rid=3332043&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20194727%26dopt%3DAbstract</link>
            <description>In conclusion, testosterone rapidly induces NO production via AR-dependent activation of eNOS in HAEC. Activation of PI3-kinase/Akt signaling and the direct interaction of AR with p85alpha are involved, at least in part, in eNOS phosphorylation.
    PMID: 20194727 [PubMed - as supplied by publisher] (Source: Endocrinology)</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3332043</comments>
            <pubDate>Mon, 01 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3332043</guid>        </item>
        <item>
            <title>Aromatase Deficiency Inhibits the Permeability Transition in Mouse Liver Mitochondria.</title>
            <link>http://www.medworm.com/index.php?rid=3332042&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20194728%26dopt%3DAbstract</link>
            <description>Authors: Moro L, Arbini AA, Hsieh JT, Ford J, Simpson ER, Hajibeigi A, Oz OK
    Lack of estrogens affects male physiology in a number of ways, including severe changes in liver metabolism that result in lipid accumulation and massive hepatic steatosis. Here we investigated whether estrogen deficiency may alter the functionality and permeability properties of liver mitochondria using, as an experimental model, aromatase knockout (ArKO) male mice, which cannot synthesize endogenous estrogens due to a disruption of the Cyp19 gene. Liver mitochondria isolated from ArKO mice displayed increased activity of the mitochondrial respiratory complex IV compared with wild-type mice and were less prone to undergo cyclosporin A-sensitive mitochondrial permeability transition (MPT) induced by calcium lo...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3332042</comments>
            <pubDate>Mon, 01 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3332042</guid>        </item>
        <item>
            <title>Functional Significance of Nuclear Estrogen Receptor Subtypes in the Liver of Goldfish.</title>
            <link>http://www.medworm.com/index.php?rid=3332041&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20194729%26dopt%3DAbstract</link>
            <description>Authors: Nelson ER, Habibi HR
    Estrogens work by binding to and activating specific estrogen receptors (ERs). Although mammals have two major nuclear ER subtypes (ERalpha and ERbeta), three subtypes have been shown in teleost fish (ERalpha, ERbeta-I, and ERbeta-II). 17beta-Estradiol stimulates the production of an egg yolk precursor protein (vitellogenin) in the liver of oviparous species, including the goldfish. However, the functional involvement of the ER subtypes in this process is not fully understood. Here, using primary goldfish hepatocytes, we test the hypothesis that all three ER subtypes are functionally involved in the liver of goldfish by using RNA interference to specifically knock-down the different ER subtypes. The results suggest that ERalpha is induced by estradiol thro...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3332041</comments>
            <pubDate>Mon, 01 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3332041</guid>        </item>
        <item>
            <title>Early Overnutrition Results in Early-Onset Arcuate Leptin Resistance and Increased Sensitivity to High-Fat Diet.</title>
            <link>http://www.medworm.com/index.php?rid=3332040&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20194730%26dopt%3DAbstract</link>
            <description>In conclusion, CPO mice exhibited early and persistent leptin resistance in the arcuate nucleus and, in response to HFD, rapid development of obesity and insulin resistance. These studies suggest that early overnutrition can permanently alter energy homeostasis and significantly increase susceptibility to obesity and insulin resistance.
    PMID: 20194730 [PubMed - as supplied by publisher] (Source: Endocrinology)</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3332040</comments>
            <pubDate>Mon, 01 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3332040</guid>        </item>
        <item>
            <title>Thyroid Hormone Receptor {alpha} Modulates Lipopolysaccharide-Induced Changes in Peripheral Thyroid Hormone Metabolism.</title>
            <link>http://www.medworm.com/index.php?rid=3332039&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20194731%26dopt%3DAbstract</link>
            <description>Authors: Kwakkel J, Chassande O, van Beeren HC, Fliers E, Wiersinga WM, Boelen A
    Acute inflammation is characterized by low serum T3 and T4 levels accompanied by changes in liver type 1 deiodinase (D1), liver D3, muscle D2, and muscle D3 expression. It is unknown at present whether thyroid hormone receptor alpha (TRalpha) plays a role in altered peripheral thyroid hormone metabolism during acute illness in vivo. We induced acute illness in TRalpha-deficient (TRalpha(0/0)) mice by administration of a sublethal dose of LPS. Compared with wild-type, TRalpha(0/0) mice have lower basal serum T4 and lower liver D1 activity and muscle D3 mRNA expression, whereas liver D3 activity is higher. These changes are gender specific. The inflammatory response to LPS was similar in WT and TRalpha(0/0) ...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3332039</comments>
            <pubDate>Mon, 01 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3332039</guid>        </item>
        <item>
            <title>Does short-term estrogen therapy produce lasting benefits in brain?</title>
            <link>http://www.medworm.com/index.php?rid=3298799&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20172970%26dopt%3DAbstract</link>
            <description>Authors: Gibbs RB
    
    PMID: 20172970 [PubMed - in process] (Source: Endocrinology)</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3298799</comments>
            <pubDate>Tue, 23 Feb 2010 19:34:15 +0100</pubDate>
            <guid isPermaLink="false">3298799</guid>        </item>
        <item>
            <title>Whatever way weight goes, inflammation shows.</title>
            <link>http://www.medworm.com/index.php?rid=3298798&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20172971%26dopt%3DAbstract</link>
            <description>Authors: Clarke IJ
    
    PMID: 20172971 [PubMed - in process] (Source: Endocrinology)</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3298798</comments>
            <pubDate>Tue, 23 Feb 2010 19:34:13 +0100</pubDate>
            <guid isPermaLink="false">3298798</guid>        </item>
        <item>
            <title>&quot;Sumer is icumen in:&quot; lessons from the lungfish.</title>
            <link>http://www.medworm.com/index.php?rid=3298797&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20172972%26dopt%3DAbstract</link>
            <description>Authors: Funder J
    
    PMID: 20172972 [PubMed - in process] (Source: Endocrinology)</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3298797</comments>
            <pubDate>Tue, 23 Feb 2010 19:34:10 +0100</pubDate>
            <guid isPermaLink="false">3298797</guid>        </item>
        <item>
            <title>Gut-brain communications: not the same at all ages.</title>
            <link>http://www.medworm.com/index.php?rid=3298796&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20172973%26dopt%3DAbstract</link>
            <description>Authors: Banks WA
    
    PMID: 20172973 [PubMed - in process] (Source: Endocrinology)</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3298796</comments>
            <pubDate>Tue, 23 Feb 2010 19:34:08 +0100</pubDate>
            <guid isPermaLink="false">3298796</guid>        </item>
        <item>
            <title>TORC: A New Twist on Corticotropin-Releasing Hormone Gene Expression.</title>
            <link>http://www.medworm.com/index.php?rid=3298795&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20172974%26dopt%3DAbstract</link>
            <description>Authors: Spencer RL, Weiser MJ
    
    PMID: 20172974 [PubMed - in process] (Source: Endocrinology)</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3298795</comments>
            <pubDate>Tue, 23 Feb 2010 19:34:05 +0100</pubDate>
            <guid isPermaLink="false">3298795</guid>        </item>
        <item>
            <title>Glucagon-Like Peptide (GLP)-1(9-36)Amide-Mediated Cytoprotection Is Blocked by Exendin(9-39) Yet Does Not Require the Known GLP-1 Receptor.</title>
            <link>http://www.medworm.com/index.php?rid=3298803&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20172966%26dopt%3DAbstract</link>
            <description>Authors: Ban K, Kim KH, Cho CK, Sauv&amp;#xE9; M, Diamandis EP, Backx PH, Drucker DJ, Husain M
    The widely expressed dipeptidyl peptidase-4 enzyme rapidly cleaves the gut hormone glucagon-like peptide-1 [GLP-1(7-36)amide] at the N terminus to generate GLP-1(9-36)amide. Both intact GLP-1(7-36)amide and GLP-1(9-36)amide exert cardioprotective actions in rodent hearts; however, the mechanisms underlying the actions of GLP-1(9-36)amide remain poorly understood. We used mass spectrometry of coronary effluents to demonstrate that isolated mouse hearts rapidly convert infused GLP-1(7-36)amide to GLP-1(9-36)amide. After ischemia-reperfusion (I/R) injury of isolated mouse hearts, administration of GLP-1(9-36)amide or exendin-4 improved functional recovery and reduced infarct size. The direct actions...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3298803</comments>
            <pubDate>Fri, 19 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3298803</guid>        </item>
        <item>
            <title>Altered Metabolism and Lipodystrophy in the Early B-Cell Factor 1-Deficient Mouse.</title>
            <link>http://www.medworm.com/index.php?rid=3298802&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20172967%26dopt%3DAbstract</link>
            <description>In conclusion, the Ebf1-deficient animals exhibit defects in adipose tissue deposition with increased marrow adiposity and impaired glucose mobilization.
    PMID: 20172967 [PubMed - as supplied by publisher] (Source: Endocrinology)</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3298802</comments>
            <pubDate>Fri, 19 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3298802</guid>        </item>
        <item>
            <title>Female Mice Expressing Constitutively Active Mutants of FSH Receptor Present with a Phenotype of Premature Follicle Depletion and Estrogen Excess.</title>
            <link>http://www.medworm.com/index.php?rid=3298801&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20172968%26dopt%3DAbstract</link>
            <description>Authors: Peltoketo H, Strauss L, Karjalainen R, Zhang M, Stamp GW, Segaloff DL, Poutanen M, Huhtaniemi IT
    Strong gain-of-function mutations have not been identified in humans in the FSH receptor (FSHR), whereas such mutations are common among many other G protein-coupled receptors. In order to predict consequences of such mutations on humans, we first identified constitutively activated mutants of the mouse (m) Fshr and then expressed them under the human anti-M&amp;#xFC;llerian hormone promoter in transgenic mice or created knock-in mutation into the mouse genome. We show here that mutations of Asp580 in the mFSHR significantly increase the basal receptor activity. D580H and D580Y mutations of mFSHR bind FSH, but the activity of the former is neither ligand-dependent nor promiscuous towar...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3298801</comments>
            <pubDate>Fri, 19 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3298801</guid>        </item>
        <item>
            <title>Transforming Growth Factor-{beta} (TGF{beta}) Receptors I/II Differentially Regulate TGF{beta}1 and IGF-Binding Protein-3 Mitogenic Effects in the Human Placenta.</title>
            <link>http://www.medworm.com/index.php?rid=3298800&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20172969%26dopt%3DAbstract</link>
            <description>This study demonstrates that both TGFbeta1 and IGFBP-3 signal through TbetaRI/II to influence human cytotrophoblast proliferation. However, downstream pathways are distinct, because IGFBP-3 acts only through Smad-2, whereas TGFbeta1 also phosphorylates ERK, resulting in opposite effects on cytotrophoblast proliferation. The effects of maternal growth signals on placental growth and function therefore depend on the balance of ligands, receptors, and signaling molecules at the syncytiotrophoblast surface. Therapeutic manipulation of this balance might offer a strategy to optimize placental development and pregnancy outcome.
    PMID: 20172969 [PubMed - as supplied by publisher] (Source: Endocrinology)</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3298800</comments>
            <pubDate>Fri, 19 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3298800</guid>        </item>
        <item>
            <title>Characterization of the Potent Gonadotropin-Releasing Activity of RF9, a Selective Antagonist of RF-Amide-Related Peptides and Neuropeptide FF Receptors: Physiological and Pharmacological Implications.</title>
            <link>http://www.medworm.com/index.php?rid=3288557&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20160130%26dopt%3DAbstract</link>
            <description>Authors: Pineda R, Garcia-Galiano D, Sanchez-Garrido MA, Romero M, Ruiz-Pino F, Aguilar E, Dijcks FA, Blomenr&amp;#xF6;hr M, Pinilla L, van Noort PI, Tena-Sempere M
    Identification of RF-amide-related peptides (RFRP), as putative mammalian orthologs of the avian gonadotropin-inhibitory hormone, has drawn considerable interest on its potential effects and mechanisms of action in the control of gonadotropin secretion in higher vertebrates. Yet, these analyses have so far relied mostly on indirect approaches, while direct assessment of their physiological roles has been hampered by the lack of suitable antagonists. RF9 was recently reported as a selective and potent antagonist of the receptors for RFRP (RFRPR) and the related neuropeptides, neuropeptide FF (NPFF) and neuropeptide AF (NPFF rece...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3288557</comments>
            <pubDate>Tue, 16 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3288557</guid>        </item>
        <item>
            <title>Human Cytochrome P450c17: Single Step Purification and Phosphorylation of Serine 258 by Protein Kinase A.</title>
            <link>http://www.medworm.com/index.php?rid=3288556&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20160131%26dopt%3DAbstract</link>
            <description>We describe a modified strategy for preparing P450c17 in which the traditional carboxy-terminal 4xHis tag is replaced by 3xGly6xHis. This construct permits more rotational freedom of the protein when bound to the nickel affinity column, reducing steric associations between the protein and the column, and permitting a single-step chromatographic purification to apparent homogeneity. Using this vector, we explored P450c17 phosphorylation by mutagenesis of Ser and/or Thr residues to Asp or Glu to mimic the approximate size and charge of phospho-Ser or phospho-Thr. This strategy did not identify Ser and/or Thr site(s) that increase the ratio of lyase to hydroxylase activity, suggesting that the regulatory phosphorylation strategy of human P450c17 is very complicated. Although previous work has...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3288556</comments>
            <pubDate>Tue, 16 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3288556</guid>        </item>
        <item>
            <title>A Locus on Mouse Chromosome 2 Is Involved in Susceptibility to Congenital Hypothyroidism and Contains an Essential Gene Expressed in Thyroid.</title>
            <link>http://www.medworm.com/index.php?rid=3288555&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20160132%26dopt%3DAbstract</link>
            <description>We report here the mapping of a chromosomal region responsible for strain-specific development of congenital hypothyroidism in mice heterozygous for null mutations in genes encoding Nkx2-1/Titf1 and Pax8. The two strains showing a differential predisposition to congenital hypothyroidism contain several single-nucleotide polymorphisms in this locus, one of which leads to a nonsynonymous amino acid change in a highly conserved region of Dnajc17, a member of the type III heat-shock protein-40 (Hsp40) family. We demonstrate that Dnajc17 is highly expressed in the thyroid bud and had an essential function in development, suggesting an important role of this protein in organogenesis and/or function of the thyroid gland.
    PMID: 20160132 [PubMed - as supplied by publisher] (Source: Endocrinolog...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3288555</comments>
            <pubDate>Tue, 16 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3288555</guid>        </item>
        <item>
            <title>Protein Malnutrition during Pregnancy in C57BL/6J Mice Results in Offspring with Altered Circadian Physiology before Obesity.</title>
            <link>http://www.medworm.com/index.php?rid=3288554&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20160133%26dopt%3DAbstract</link>
            <description>Authors: Sutton GM, Centanni AV, Butler AA
    The mechanisms linking intrauterine growth retardation (IUGR) with adulthood obesity and diabetes are unclear. These studies investigated energy homeostasis in 8- and 20-wk-old male and female mice subjected to protein deficiency in utero. Pregnant C57BL/6J female mice were fed a protein-deficient diet (6% protein). Undernourished offspring (UO) and controls (CO) were cross-fostered to lactating dams fed a 20% control diet. The 24-h profiles of energy expenditure, feeding behavior, physical activity, and whole-body substrate preference was assessed using 8-wk UO and CO weaned onto control diet. Blood chemistries, glucose tolerance, and expression of genes involved in hepatic lipid and glucose metabolism were analyzed in 8- and 20-wk-old CO and...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3288554</comments>
            <pubDate>Tue, 16 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3288554</guid>        </item>
        <item>
            <title>Maternal Dietary Fat Determines Metabolic Profile and the Magnitude of Endocannabinoid Inhibition of the Stress Response in Neonatal Rat Offspring.</title>
            <link>http://www.medworm.com/index.php?rid=3288553&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20160134%26dopt%3DAbstract</link>
            <description>Authors: D'Asti E, Long H, Tremblay-Mercier J, Grajzer M, Cunnane SC, Di Marzo V, Walker CD
    Endocannabinoids (eCBs) are products of phospholipid (PL)-derived arachidonic acid (AA) that regulate hypothalamus-pituitary-adrenal axis activity. We hypothesized that differences in the quality and quantity of maternal dietary fat would modulate the PL AA content in the neonatal brain affecting stress responsiveness via differences in eCB production and activity in stress-activated brain areas. Pregnant rats were fed a 5% [control (C)] or 30% fat [high fat (HF)] diet rich in either n-6 (HF-n-6) or n-3 (HF-n-3) fat during the last week of gestation and lactation. Postnatal d 10 offspring were tested for metabolic hormones, AA (n-6) and eCB brain content, and hormonal effects of eCB receptor ant...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3288553</comments>
            <pubDate>Tue, 16 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3288553</guid>        </item>
        <item>
            <title>Peroxisome Proliferator-Activated Receptor-{gamma} Receptor Ligand Partially Prevents the Development of Endometrial Explants in Baboons: A Prospective, Randomized, Placebo-Controlled Study.</title>
            <link>http://www.medworm.com/index.php?rid=3288552&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20160135%26dopt%3DAbstract</link>
            <description>Authors: Lebovic DI, Mwenda JM, Chai DC, Santi A, Xu X, D'Hooghe T
    A prospective, randomized, placebo-controlled study was conducted in a baboon model to determine if a thiazolidinedione agonist of peroxisome proliferator-activated receptor-gamma, pioglitazone, can impede the development of endometriosis. Endometriosis was induced using laparoscopic, intrapelvic injection of eutopic menstrual endometrium, previously incubated with placebo or pioglitazone for 30 min, in 12 female baboons with a normal pelvis that had undergone at least one menstrual cycle since the time of captivity. At this point, the 12 baboons were randomized into two groups and treated from the day of induction. They received either PBS tablets (n = 6, placebo control, placebo tablets once a day by mouth) or pioglit...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3288552</comments>
            <pubDate>Tue, 16 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3288552</guid>        </item>
        <item>
            <title>Selective Activation of Estrogen Receptor-{beta} Target Genes by 3,3'-Diindolylmethane.</title>
            <link>http://www.medworm.com/index.php?rid=3288551&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20160136%26dopt%3DAbstract</link>
            <description>Authors: Vivar OI, Saunier EF, Leitman DC, Firestone GL, Bjeldanes LF
    3,3'-Diindolylmethane (DIM) is a natural compound found in cruciferous vegetables that has antiproliferative and estrogenic activity. However, it is not clear whether the estrogenic effects are mediated through estrogen receptor (ER)alpha, ERbeta, or both ER subtypes. We investigated whether DIM has ER subtype selectivity on gene transcription. DIM stimulated ERbeta but not ERalpha activation of an estrogen response element upstream of the luciferase reporter gene. DIM also selectively activated multiple endogenous genes through ERbeta. DIM did not bind to ERbeta, indicating that it activates genes by a ligand-independent mechanism. DIM causes ERbeta to bind regulatory elements and recruit the steroid receptor coacti...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3288551</comments>
            <pubDate>Tue, 16 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3288551</guid>        </item>
        <item>
            <title>Individual Differences in Reactivity to Social Stress Predict Susceptibility and Resilience to a Depressive Phenotype: Role of Corticotropin-Releasing Factor.</title>
            <link>http://www.medworm.com/index.php?rid=3288550&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20160137%26dopt%3DAbstract</link>
            <description>Authors: Wood SK, Walker HE, Valentino RJ, Bhatnagar S
    Previous social stress exposure is a common risk factor for affective disorders. However, factors that determine vulnerability or resiliency to social stress-induced psychopathologies remain unclear. Using a rodent model of social stress, the present study was designed to identify putative neurobiological substrates that contribute to social stress-induced psychopathology and factors that influence or predict vulnerability. The resident-intruder model of defeat was used as a social stressor in adult male Sprague Dawley rats. The average latency to assume a subordinate posture (signaling defeat) over seven daily defeat exposures was calculated and examined with respect to endpoints of hypothalamic-pituitary-adrenal activity, compone...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3288550</comments>
            <pubDate>Tue, 16 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3288550</guid>        </item>
        <item>
            <title>Maternal Leukemia Inhibitory Factor (LIF) Promotes Fetal Neurogenesis via a LIF-ACTH-LIF Signaling Relay Pathway.</title>
            <link>http://www.medworm.com/index.php?rid=3288549&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20160138%26dopt%3DAbstract</link>
            <description>Authors: Simamura E, Shimada H, Higashi N, Uchishiba M, Otani H, Hatta T
    Leukemia inhibitory factor (LIF) promotes the proliferation of neuronal progenitor cells in the cerebrum. However, it remains unclear how fetal LIF level is regulated. Here we show evidence that maternal LIF signals drive fetal LIF levels via the placenta, thereby promoting neurogenesis in the fetal brain in rats. Chronological changes showed that LIF concentration in fetal sera (FS) and fetal cerebrospinal fluid peaked at gestational day (GD) 15.5, after the peak of maternal LIF at GD14.5. LIF injection into rat dams at GD15.5 increased the level of ACTH in FS and subsequently increased LIF levels in FS and fetal cerebrospinal fluid. The elevation of fetal LIF after LIF injection into dams was inhibited by in ute...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3288549</comments>
            <pubDate>Tue, 16 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3288549</guid>        </item>
        <item>
            <title>Epidermal Growth Factor Stimulates Human Trophoblast Cell Migration through Rho A and Rho C Activation.</title>
            <link>http://www.medworm.com/index.php?rid=3270310&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20150581%26dopt%3DAbstract</link>
            <description>This study investigated the roles of Rho protein in epidermal growth factor (EGF)-induced trophoblast cell migration and its mechanism. Using choriocarcinoma cell lines JEG-3 and JAR and first-trimester human chorionic villus explant cultures on matrigel, we examined EGF-mediated stimulation of trophoblast migration. EGF is shown to have a dose-dependent effect on trophoblast migration. A low concentration of EGF (1 ng/ml) has a stimulatory effect on cell migration, whereas high concentrations of EGF (100 ng/ml) shows an inhibitory effect. EGF (1 ng/ml) activates RhoA and RhoC, but not RhoB, through elevated protein levels and activity. EGF-induced migration was shown to be inhibited by either cell-permeable C3 exoenzyme transferase or selective RhoA or RhoC small interfering RNAs. The inh...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3270310</comments>
            <pubDate>Thu, 11 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3270310</guid>        </item>
        <item>
            <title>Nuclear Targeting of Cyclin-Dependent Kinase 2 Reveals Essential Roles of Cyclin-Dependent Kinase 2 Localization and Cyclin E in Vitamin D-Mediated Growth Inhibition.</title>
            <link>http://www.medworm.com/index.php?rid=3264107&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20147522%26dopt%3DAbstract</link>
            <description>In this study, we investigated the role of CDK2 cytoplasmic relocalization in the antiproliferative effects of 1,25-(OH)2D3. CDK2 was found to be necessary for prostate cancer cell proliferation. Although induced by 1,25-(OH)2D3, the cyclin-dependent kinase inhibitor p27(KIP1) was dispensable for 1,25-(OH)2D3-mediated growth inhibition. Reduction in CDK2 activity by 1,25-(OH)2D3 was associated with decreased T160 phosphorylation, a residue whose phosphorylation in the nucleus is essential for CDK2 activity. Ectopic expression of cyclin E was sufficient to overcome 1,25-(OH)2D3-mediated cytoplasmic mislocalization of CDK2 and all antiproliferative effects of 1,25-(OH)2D3, yet endogenous levels of cyclin E or binding to CDK2 were not affected by 1,25-(OH)2D3. Similarly, knockdown of the CDK2...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3264107</comments>
            <pubDate>Wed, 10 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3264107</guid>        </item>
        <item>
            <title>Vasotocin/V2-Type Receptor/Aquaporin Axis Exists in African Lungfish Kidney but Is Functional Only in Terrestrial Condition.</title>
            <link>http://www.medworm.com/index.php?rid=3264106&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20147523%26dopt%3DAbstract</link>
            <description>Authors: Konno N, Hyodo S, Yamaguchi Y, Matsuda K, Uchiyama M
    The vasopressin/vasotocin (VT)-V2-type receptor (V2R)-aquaporin (AQP)-2 axis plays a pivotal role in renal water reabsorption in tetrapods. It is widely thought that this axis evolved with the emergence of the tetrapods, reflecting a requirement of water retention in terrestrial environment. Here we report that lungfish, the closest living relatives of tetrapods, already possess a system similar to the VT-V2R-AQP2 axis in the kidney, but the system is functional only in the terrestrial estivating condition. We cloned a novel AQP paralogous to AQP0. The water permeability of Xenopus oocytes was increased by injection with the AQP cRNA and was further facilitated by preincubation with cAMP. In the kidney of estivating lungfish...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3264106</comments>
            <pubDate>Wed, 10 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3264106</guid>        </item>
        <item>
            <title>Disruption of the Dopamine D2 Receptor Impairs Insulin Secretion and Causes Glucose Intolerance.</title>
            <link>http://www.medworm.com/index.php?rid=3264105&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20147524%26dopt%3DAbstract</link>
            <description>Authors: Garc&amp;#xED;a-Tornad&amp;#xFA; I, Ornstein AM, Chamson-Reig A, Wheeler MB, Hill DJ, Arany E, Rubinstein M, Becu-Villalobos D
    The relationship between antidopaminergic drugs and glucose has not been extensively studied, even though chronic neuroleptic treatment causes hyperinsulinemia in normal subjects or is associated with diabetes in psychiatric patients. We sought to evaluate dopamine D2 receptor (D2R) participation in pancreatic function. Glucose homeostasis was studied in D2R knockout mice (Drd2(-/-)) mice and in isolated islets from wild-type and Drd2(-/-) mice, using different pharmacological tools. Pancreas immunohistochemistry was performed. Drd2(-/-) male mice exhibited an impairment of insulin response to glucose and high fasting glucose levels and were glucose intolerant...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3264105</comments>
            <pubDate>Wed, 10 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3264105</guid>        </item>
        <item>
            <title>1{alpha},25-Dihydroxyvitamin D3 Inhibits Growth of VCaP Prostate Cancer Cells Despite Inducing the Growth-Promoting TMPRSS2:ERG Gene Fusion.</title>
            <link>http://www.medworm.com/index.php?rid=3264104&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20147525%26dopt%3DAbstract</link>
            <description>Authors: Washington MN, Weigel NL
    Vitamin D receptor (VDR) agonists have been shown to reduce the growth of several prostate cancer cell lines. However, the effects of VDR activation have not been examined in the presence of the recently identified androgen-regulated TMPRSS2:ERG gene fusions, which occur in a high percentage of prostate cancers and play a role in growth and invasiveness. In a previous microarray study, we found that VDR activation induces TMPRSS2 expression in LNCaP prostate cancer cells. Here we show that the natural VDR agonist 1alpha,25-dihydroxyvitamin D3 and its synthetic analog EB1089 increase expression of TMPRSS2:ERG mRNA in VCaP prostate cancer cells; this results in increased ETS-related gene (ERG) protein expression and ERG activity as demonstrated by an inc...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3264104</comments>
            <pubDate>Wed, 10 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3264104</guid>        </item>
        <item>
            <title>The Effect of Dietary Protein on Intestinal Calcium Absorption in Rats.</title>
            <link>http://www.medworm.com/index.php?rid=3264103&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20147526%26dopt%3DAbstract</link>
            <description>Authors: Gaffney-Stomberg E, Sun BH, Cucchi CE, Simpson CA, Gundberg C, Kerstetter JE, Insogna KL
    Increaing dietary protein intake in humans acutely increases urinary calcium. Isotopic absorption studies have indicated that, at least in the short term, this is primarily due to increased intestinal Ca absorption. To explore the mechanisms underlying dietary protein's effect on intestinal Ca absorption, female Sprague Dawley rats were fed a control (20%), low (5%), or high (40%) protein diet for 7 d, and Ca balance was measured during d 4-7. On d 7, duodenal mucosa was harvested and brush border membrane vesicles (BBMVs) were prepared to evaluate Ca uptake. By d 7, urinary calcium was more than 2-fold higher in the 40% protein group compared with control (4.2 mg/d vs. 1.7 mg/d; P &amp;lt; 0....</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3264103</comments>
            <pubDate>Wed, 10 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3264103</guid>        </item>
        <item>
            <title>15-Deoxy-{Delta}12-14-Prostaglandin-J2 Induces Hypertrophy and Loss of Contractility in Human Testicular Peritubular Cells: Implications for Human Male Fertility.</title>
            <link>http://www.medworm.com/index.php?rid=3247353&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20133451%26dopt%3DAbstract</link>
            <description>Authors: Schell C, Albrecht M, Spillner S, Mayer C, Kunz L, K&amp;#xF6;hn FM, Schwarzer U, Mayerhofer A
    The wall of the seminiferous tubules contains contractile smooth-muscle-like peritubular cells, thought to be important for sperm transport. Impaired spermatogenesis in men typically involves remodeling of this wall, and we now found that smooth muscle cell (SMC) markers, namely myosin heavy chain (MYH11) and smooth muscle actin (SMA) are often lost or diminished in peritubular cells of testes of men with impaired spermatogenesis. This suggests reduced contractility of the peritubular wall, which may contribute to sub- or infertility. In these cases, testicular expression of cyclooxygenase-2 (COX-2) implies formation of prostaglandins (PGs). When screening different PGs for their ability...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3247353</comments>
            <pubDate>Thu, 04 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3247353</guid>        </item>
        <item>
            <title>Prenatal Dexamethasone Programs Expression of Genes in Liver and Adipose Tissue and Increased Hepatic Lipid Accumulation But Not Obesity on a High-Fat Diet.</title>
            <link>http://www.medworm.com/index.php?rid=3247352&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20133452%26dopt%3DAbstract</link>
            <description>Authors: Drake AJ, Raubenheimer PJ, Kerrigan D, McInnes KJ, Seckl JR, Walker BR
    The association between low birth weight and cardiovascular disease is amplified by the development of obesity. We explored the effects of postnatal high-fat (HF) feeding in dexamethasone (Dex)-programmed rats, in which prenatal glucocorticoid overexposure is associated with reduced birth weight and adult glucose intolerance. Male Wistar rats exposed to Dex or vehicle (Veh) during the last week of gestation were weaned onto HF or control diets for 6 months. Dex-exposed animals were of lower birth weight and showed catch-up growth by 7 wk. There were no differences in obesity or hyperinsulinaemia between Dex-HF and Veh-HF animals. However, Dex-HF animals had increased hepatic triglyceride content compared wi...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3247352</comments>
            <pubDate>Thu, 04 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3247352</guid>        </item>
        <item>
            <title>Growth Activation Alone Is Not Sufficient to Cause Metastatic Thyroid Cancer in a Mouse Model of Follicular Thyroid Carcinoma.</title>
            <link>http://www.medworm.com/index.php?rid=3247351&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20133453%26dopt%3DAbstract</link>
            <description>Authors: Lu C, Zhao L, Ying H, Willingham MC, Cheng SY
    TSH is the major stimulator of thyrocyte proliferation, but its role in thyroid carcinogenesis remains unclear. To address this question, we used a mouse model of follicular thyroid carcinoma (FTC) (TRbeta(PV/PV) mice). These mice, harboring a dominantly negative mutation (PV) of the thyroid hormone-beta receptor (TRbeta), exhibit increased serum thyroid hormone and elevated TSH. To eliminate TSH growth-stimulating effect, TRbeta(PV/PV) mice were crossed with TSH receptor gene knockout (TSHR(-/-)) mice. Wild-type siblings of TRbeta(PV/PV) mice were treated with an antithyroid agent, propylthiouracil, to elevate serum TSH for evaluating long-term TSH effect (WT-PTU mice). Thyroids from TRbeta(PV/PV)TSHR(-/-) showed impaired growth w...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3247351</comments>
            <pubDate>Thu, 04 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3247351</guid>        </item>
        <item>
            <title>The Levels of the Endocannabinoid Receptor CB2 and Its Ligand 2-Arachidonoylglycerol Are Elevated in Endometrial Carcinoma.</title>
            <link>http://www.medworm.com/index.php?rid=3247350&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20133454%26dopt%3DAbstract</link>
            <description>In conclusion, the endocannabinoid system seems to play an important role in human endometrial carcinoma, and modulation of CB2 activity/expression may account for a tumor-suppressive effect.
    PMID: 20133454 [PubMed - as supplied by publisher] (Source: Endocrinology)</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3247350</comments>
            <pubDate>Thu, 04 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3247350</guid>        </item>
        <item>
            <title>Role of Estradiol in the Dynamic Control of Tanycyte Plasticity Mediated by Vascular Endothelial Cells in the Median Eminence.</title>
            <link>http://www.medworm.com/index.php?rid=3247349&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20133455%26dopt%3DAbstract</link>
            <description>Authors: de Seranno S, d'Anglemont de Tassigny X, Estrella C, Loyens A, Kasparov S, Leroy D, Ojeda SR, Beauvillain JC, Prevot V
    In the ever-changing physiological context of the neuroendocrine brain, the mechanisms by which cellular events involving neurons, astroglia, and vascular cells are coordinated to bring forth the appropriate neuronal signaling is not yet known but is amenable to examination. In the median eminence of the hypothalamus, endothelial cells are key players in the plasticity of tanycytes (specialized astroglia) and neuroendocrine synapse efficacy. Here we report that estradiol acts on both purified endothelial cells and isolated tanycytes to trigger endothelial-to-glial communication that leads to a sudden and massive retraction of tanycyte processes. The blockade o...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3247349</comments>
            <pubDate>Thu, 04 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3247349</guid>        </item>
        <item>
            <title>Adenosine 5'-Monophosphate-Activated Protein Kinase-Mammalian Target of Rapamycin Cross Talk Regulates Brown Adipocyte Differentiation.</title>
            <link>http://www.medworm.com/index.php?rid=3247348&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20133456%26dopt%3DAbstract</link>
            <description>This study demonstrates a critical role for AMPK in controlling the mTOR-p70S6K1 signaling cascade in brown but not in 3T3-L1 adipocytes. We observed that mTOR activity is essential in the first stages of differentiation. Nevertheless, subsequent inhibition of this cascade by AMPK activation is also necessary at later stages. An in vivo study showed that prolonged 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR)-induced AMPK activation increases uncoupling protein 1 expression and induces an accumulation of brown adipocytes in white adipose tissue (WAT), as revealed by immunohistology. Moreover, the induction of brown adipogenesis in areas of white fat partially correlates with the body weight reduction detected in response to treatment with AICAR. Taken together, our study reveals th...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3247348</comments>
            <pubDate>Thu, 04 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3247348</guid>        </item>
        <item>
            <title>Minireview: Mechano-Growth Factor: A Putative Product of IGF-I Gene Expression Involved in Tissue Repair and Regeneration.</title>
            <link>http://www.medworm.com/index.php?rid=3247357&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20130113%26dopt%3DAbstract</link>
            <description>Authors: Matheny RW, Nindl BC, Adamo ML
    The discovery that IGF-I mRNAs encoding isoforms of the pro-IGF-I molecule are differentially regulated in response to mechanical stress in skeletal muscle has been the impetus for a number of studies designed to demonstrate that alternative splicing of IGF-I pre-mRNA involving exons 4, 5, and 6 gives rise to a unique peptide derived from pro-IGF-I that plays a novel role in myoblast proliferation. Research suggests that after injury to skeletal muscle, the IGF-IEb mRNA splice variant is up-regulated initially, followed by up-regulation of the IGF-IEa splice variant at later time points. Up-regulation of IGF-IEb mRNA correlates with markers of satellite cell and myoblast proliferation, whereas up-regulation of IGF-IEa mRNA is correlated with diff...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3247357</comments>
            <pubDate>Wed, 03 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3247357</guid>        </item>
        <item>
            <title>Toll-Like Receptor Ligands Cause Proinflammatory and Prodiabetic Activation of Adipocytes via Phosphorylation of Extracellular Signal-Regulated Kinase and c-Jun N-Terminal Kinase But Not Interferon Regulatory Factor-3.</title>
            <link>http://www.medworm.com/index.php?rid=3247356&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20130114%26dopt%3DAbstract</link>
            <description>Authors: Kopp A, Buechler C, Bala M, Neumeier M, Sch&amp;#xF6;lmerich J, Sch&amp;#xE4;ffler A
    Here, we aim to investigate the mechanisms of Toll-like receptor (TLR)-induced prodiabetic and proinflammatory activation of adipocytes and to detect differences in the responsiveness of TLRs to their respective ligands between adipocytes isolated from inflamed vs. noninflamed adipose tissue. Experiments using specific ligands for all known TLRs were performed in murine 3T3-L1 adipocytes and in human adipocytes isolated from noninflamed and inflamed adipose tissue. IL-6 and monocyte chemoattractant protein-1 (MCP-1) release were measured by ELISA. The expression of the signal transduction proteins phospho-extracellular signal-regulated kinase (P-Erk), P-c-Jun N-terminal kinase (JNK), and P-interferon ...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3247356</comments>
            <pubDate>Wed, 03 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3247356</guid>        </item>
        <item>
            <title>Hydroxysteroid (17{beta}) Dehydrogenase 12 Is Essential for Mouse Organogenesis and Embryonic Survival.</title>
            <link>http://www.medworm.com/index.php?rid=3247355&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20130115%26dopt%3DAbstract</link>
            <description>Authors: Rantakari P, Lagerbohm H, Kaimainen M, Suomela JP, Strauss L, Sainio K, Pakarinen P, Poutanen M
    Hydroxysteroid (17beta) dehydrogenases (HSD17Bs) have a significant role in steroid metabolism by catalyzing the conversion between 17-keto and 17beta-hydroxysteroids. However, several studies in vitro have shown that some of these enzymes may also be involved in other metabolic pathways. Among these enzymes, HSD17B12 has been shown to be involved in both the biosynthesis of estradiol and the elongation of the essential very long fatty acids in vitro and in vivo. To investigate the function of mammalian HSD17B12 in vivo, we generated mice with a null mutation of the Hsd17b12 gene (HSD17B12KO mice) by using a gene-trap vector, resulting in the expression of the lacZ gene of the trapp...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3247355</comments>
            <pubDate>Wed, 03 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3247355</guid>        </item>
        <item>
            <title>Intestinal and Hepatic Cholesterol Carriers in Diabetic Psammomys obesus.</title>
            <link>http://www.medworm.com/index.php?rid=3247354&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20130116%26dopt%3DAbstract</link>
            <description>Authors: Levy E, Lalonde G, Delvin E, Elchebly M, Pr&amp;#xE9;court LP, Seidah NG, Spahis S, Rabasa-Lhoret R, Ziv E
    Insulin resistance and type 2 diabetes (T2D) are characterized by hyperlipidemia. The aim of the present study was to elucidate whether T2D contributes to abnormal cholesterol (CHOL) homeostasis. Experiments were carried out in the small intestine and liver of Psammomys obesus, a model of nutritionally induced T2D. Our results show that diabetic animals exhibited a lower intestinal CHOL uptake, which was associated with a decrease in 1) the gene and protein expression of Niemann-Pick C1 like 1 that plays a pivotal role in CHOL incorporation in the enterocytes; and 2) mRNA of ATP-binding cassette transporters (ABC)A1 that mediates CHOL efflux from intestinal cells to apolipopr...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3247354</comments>
            <pubDate>Wed, 03 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3247354</guid>        </item>
        <item>
            <title>Expecting to eat: glucagon-like peptide-1 and the anticipation of meals.</title>
            <link>http://www.medworm.com/index.php?rid=3214488&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20100914%26dopt%3DAbstract</link>
            <description>Authors: Williams DL
    
    PMID: 20100914 [PubMed - in process] (Source: Endocrinology)</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3214488</comments>
            <pubDate>Thu, 28 Jan 2010 15:06:14 +0100</pubDate>
            <guid isPermaLink="false">3214488</guid>        </item>
        <item>
            <title>Antagonizing kisspeptins: physiological lessons and pharmacological challenges.</title>
            <link>http://www.medworm.com/index.php?rid=3214487&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20100915%26dopt%3DAbstract</link>
            <description>Authors: Vaudry H
    
    PMID: 20100915 [PubMed - in process] (Source: Endocrinology)</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3214487</comments>
            <pubDate>Thu, 28 Jan 2010 15:06:04 +0100</pubDate>
            <guid isPermaLink="false">3214487</guid>        </item>
        <item>
            <title>Isolation of Human Adrenocortical Aldosterone-Producing Cells by a Novel Immunomagnetic Beads Method.</title>
            <link>http://www.medworm.com/index.php?rid=3208795&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20097714%26dopt%3DAbstract</link>
            <description>Authors: Caroccia B, Fassina A, Seccia TM, Recarti C, Petrelli L, Belloni AS, Pelizzo MR, Rossi GP
    We detected intense CD56 immunostaining in the zona glomerulosa (ZG) and medulla of the normal human adrenal gland and therefore identified CD56, the neural cell adhesion molecule, as a membrane antigen specific for the ZG, aldosterone-producing adenoma (APA), and chromaffin cells. The APA and pheochromocytoma cells, which are histogenetically derived from the ZG and medulla, respectively, also showed intense CD56 immunostaining. Based on these findings we developed a strategy for isolating cells from the ZG and APA using CD56 immunobinding to magnetic beads. Morphology, gene expression studies, and aldosterone measurement confirmed that CD56 positive (+) cells were ZG and APA cells. Anal...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3208795</comments>
            <pubDate>Fri, 22 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3208795</guid>        </item>
        <item>
            <title>Hypothalamic Insulin-Like Growth Factor-I Receptors Are Necessary for Hormone-Dependent Luteinizing Hormone Surges: Implications for Female Reproductive Aging.</title>
            <link>http://www.medworm.com/index.php?rid=3208794&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20097715%26dopt%3DAbstract</link>
            <description>Authors: Todd BJ, Merhi ZO, Shu J, Etgen AM, Neal-Perry GS
    Brain IGF-I receptors are required for maintenance of estrous cycles in young adult female rats. Circulating and hypothalamic IGF-I levels decrease with aging, suggesting a role for IGF-I in the onset of reproductive senescence. Therefore, the present study investigated potential mechanisms of action of brain IGF-I receptors in the regulation of LH surges in young adult and middle-aged rats. We continuously infused IGF-I, the selective IGF-I receptor antagonist JB-1, or vehicle into the third ventricle of ovariectomized young adult and middle-aged female rats primed with estradiol and progesterone. Pharmacological blockade of IGF-I receptors attenuated and delayed the LH surge in young adult rats, reminiscent of the LH surge pa...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3208794</comments>
            <pubDate>Fri, 22 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3208794</guid>        </item>
        <item>
            <title>Regulation of Aldosterone Synthase by Activator Transcription Factor/cAMP Response Element-Binding Protein Family Members.</title>
            <link>http://www.medworm.com/index.php?rid=3208793&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20097716%26dopt%3DAbstract</link>
            <description>Authors: Nogueira EF, Rainey WE
    Aldosterone synthesis is regulated by angiotensin II (Ang II) and K(+) acting in the adrenal zona glomerulosa, in part through the regulation of aldosterone synthase (CYP11B2). Here, we analyzed the role of cAMP response element (CRE)-binding proteins (CREBs) in the regulation of CYP11B2. Expression analysis of activator transcription factor (ATF)/CREB family members, namely the ATF1 and ATF2, the CREB, and the CRE modulator, in H295R cells and normal human adrenal tissue was performed using quantitative real-time PCR. Ang II-induced phosphorylation of ATF/CREB members was analyzed by Western blot analysis, and their subsequent binding to the CYP11B2 promoter using chromatin immunoprecipitation assay. Aldosterone production and CYP11B2 expression were me...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3208793</comments>
            <pubDate>Fri, 22 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3208793</guid>        </item>
        <item>
            <title>Caveolin-1 Ablation Reduces the Adverse Cardiovascular Effects of N-{omega}-Nitro-L-Arginine Methyl Ester and Angiotensin II.</title>
            <link>http://www.medworm.com/index.php?rid=3208792&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20097717%26dopt%3DAbstract</link>
            <description>Authors: Pojoga LH, Romero JR, Yao TM, Loutraris P, Ricchiuti V, Coutinho P, Guo C, Lapointe N, Stone JR, Adler GK, Williams GH
    Caveolae are the major cellular membrane structure through which extracellular mediators transmit information to intracellular signaling pathways. In vascular tissue (but not ventricular myocardium), caveolin-1 (cav-1) is the main component of caveolae; cav-1 modulates enzymes and receptors, such as the endothelial nitric oxide synthase and the angiotensin II (AngII) type 1 receptor. Evidence suggests that AngII and aldosterone (ALDO) are important mediators of ventricular injury. We have described a model of biventricular damage in rodents that relies on treatment with N-omega-nitro-L-arginine methyl ester (L-NAME (nitric oxide synthase inhibitor)) and AngII....</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3208792</comments>
            <pubDate>Fri, 22 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3208792</guid>        </item>
        <item>
            <title>Aromatase Inhibitors Induce Spine Synapse Loss in the Hippocampus of Ovariectomized Mice.</title>
            <link>http://www.medworm.com/index.php?rid=3208791&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20097718%26dopt%3DAbstract</link>
            <description>Authors: Zhou L, Fester L, von Blittersdorff B, Hassu B, Nogens H, Prange-Kiel J, Jarry H, Wegscheider K, Rune GM
    Recently, inhibition of estrogen synthesis by aromatase inhibitors has become a favored therapy for breast cancer in postmenopausal women. Estrogen is, however, important for synapse formation in the hippocampus. Inhibition of aromatase induces spine synapse loss in organotypic hippocampal slice cultures. We therefore studied the effect of systemic treatment with the potent aromatase inhibitor letrozole on spine synapse formation and synaptic proteins in the hippocampi of female mice for periods of 7 d and 4 wk. In cyclic, letrozole-treated females and in ovariectomized, letrozole-treated females, the number of spine synapses was significantly reduced in the hippocampus but...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3208791</comments>
            <pubDate>Fri, 22 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3208791</guid>        </item>
        <item>
            <title>Epidermal Growth Factor Receptor Is an Obligatory Intermediate for Oxytocin-Induced Cyclooxygenase 2 Expression and Prostaglandin F2{alpha} Production in Bovine Endometrial Epithelial Cells.</title>
            <link>http://www.medworm.com/index.php?rid=3190000&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20080869%26dopt%3DAbstract</link>
            <description>Authors: Krishnaswamy N, Lacroix-Pepin N, Chapdelaine P, Taniguchi H, Kauffenstein G, Chakravarti A, Danyod G, Fortier MA
    Oxytocin (OT) triggers the luteolytic pulses of prostaglandin F2alpha (PGF2alpha) from the endometrial epithelial cells in ruminants. We have proposed that the embryonic signal interferon-tau exerts its antiluteolytic effect by disrupting the OT signaling axis. Accordingly, we have attempted to define the signaling pathway of OT-induced PGF2alpha production in the bovine endometrium using our newly characterized epithelial cell line (bEEL). OT receptor was coupled to the classical Galphaq pathway as evidenced by calcium release and activation of phospholipase C. Similarly, OT-induced PGF2alpha production was mediated through the canonical ERK1/2 pathway. Because of ...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3190000</comments>
            <pubDate>Fri, 15 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3190000</guid>        </item>
        <item>
            <title>Disrupted Corticosterone Pulsatile Patterns Attenuate Responsiveness to Glucocorticoid Signaling in Rat Brain.</title>
            <link>http://www.medworm.com/index.php?rid=3189999&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20080870%26dopt%3DAbstract</link>
            <description>Authors: Sarabdjitsingh RA, Isenia S, Polman A, Mijalkovic J, Lachize S, Datson N, de Kloet ER, Meijer OC
    Chronically elevated circulating glucocorticoid levels are although to enhance vulnerability to psychopathology. Here we hypothesized that such sustained glucocorticoid levels, disturbing corticosterone pulsatility, attenuate glucocorticoid receptor signaling and target gene responsiveness to an acute challenge in the rat brain. Rats were implanted with vehicle or 40 or 100% corticosterone pellets known to flatten ultradian and circadian rhythmicity while maintaining daily average levels or mimic pathological conditions. Additionally, recovery from constant exposure was studied in groups that had the pellet removed 24 h prior to the challenge. Molecular markers for receptor respons...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3189999</comments>
            <pubDate>Fri, 15 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3189999</guid>        </item>
        <item>
            <title>Involvement of Transducer of Regulated cAMP Response Element-Binding Protein Activity on Corticotropin Releasing Hormone Transcription.</title>
            <link>http://www.medworm.com/index.php?rid=3189998&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20080871%26dopt%3DAbstract</link>
            <description>Authors: Liu Y, Coello AG, Grinevich V, Aguilera G
    We have recently shown that phospho-cAMP response element-binding protein (CREB) is essential but not sufficient for activation of CRH transcription, suggesting the requirement of a coactivator. Here, we test the hypothesis that the CREB coactivator, transducer of regulated CREB activity (TORC), is required for activation of CRH transcription, using the cell line 4B and primary cultures of hypothalamic neurons. Immunohistochemistry and Western blot experiments in 4B cells revealed time-dependent nuclear translocation of TORC1,TORC 2, and TORC3 by forskolin [but not by the phorbol ester, phorbol 12-myristate 13-acetate (PMA)] in a concentration-dependent manner. In reporter gene assays, cotransfection of TORC1 or TORC2 potentiated the s...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3189998</comments>
            <pubDate>Fri, 15 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3189998</guid>        </item>
        <item>
            <title>Limb Muscles Are Androgen Targets in an Acrobatic Tropical Bird.</title>
            <link>http://www.medworm.com/index.php?rid=3189997&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20080872%26dopt%3DAbstract</link>
            <description>Authors: Feng NY, Katz A, Day LB, Barske J, Schlinger BA
    Spectacular athleticism is a conspicuous feature of many animal courtship displays yet surprisingly little is known about androgen dependence of skeletal muscles underlying these displays. Testosterone (T) acts through androgen receptors (ARs) to stimulate muscular male Golden-collared manakins of Panama to perform a remarkably athletic courtship display that includes loud wingsnaps generated by the rapid and forceful lifting of the wings. We tested the hypothesis that androgen sensitivity, reflected in the expression levels of AR mRNA, is a muscular adaptation supporting these courtship displays. Quantitative PCR showed substantially greater AR mRNA expression in all limb muscles of wild male and female manakins compared with tw...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3189997</comments>
            <pubDate>Fri, 15 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3189997</guid>        </item>
        <item>
            <title>Food Intake during the Normal Activity Phase Prevents Obesity and Circadian Desynchrony in a Rat Model of Night Work.</title>
            <link>http://www.medworm.com/index.php?rid=3189996&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20080873%26dopt%3DAbstract</link>
            <description>Authors: Salgado-Delgado R, Angeles-Castellanos M, Saderi N, Buijs RM, Escobar C
    Shift work or night work is associated with hypertension, metabolic syndrome, cancer, and other diseases. The cause for these pathologies is proposed to be the dissociation between the temporal signals from the biological clock and the sleep/activity schedule of the night worker. We investigated the mechanisms promoting metabolic desynchrony in a model for night work in rats, based on daily 8-h activity schedules during the resting phase. We demonstrate that the major alterations leading to internal desynchrony induced by this working protocol, flattened glucose and locomotor rhythms and the development of abdominal obesity, were caused by food intake during the rest phase. Shifting food intake to the norm...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3189996</comments>
            <pubDate>Fri, 15 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3189996</guid>        </item>
        <item>
            <title>Thrombospondin-1 Inhibits Angiogenesis and Promotes Follicular Atresia in a Novel in Vitro Angiogenesis Assay.</title>
            <link>http://www.medworm.com/index.php?rid=3189995&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20080874%26dopt%3DAbstract</link>
            <description>Authors: Garside SA, Harlow CR, Hillier SG, Fraser HM, Thomas FH
    Thrombospondin-1 (TSP-1) is a putative antiangiogenic factor, but its role in regulating physiological angiogenesis is unclear. We have developed a novel in vitro angiogenesis assay to study the effect of TSP-1 on follicular angiogenesis and development. Intact preantral/early antral follicles dissected from 21-d-old rat ovaries were cultured for 6 d in the presence or absence of TSP-1. At the end of the culture period, angiogenic sprouting from the follicles was quantified using image analysis. Follicles were fixed and sectioned, and follicular apoptosis was assessed by immunohistochemistry for activated caspase-3 in granulosa cells. The results showed that TSP-1 inhibited follicular angiogenesis (P &amp;lt; 0.01) and promot...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3189995</comments>
            <pubDate>Fri, 15 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3189995</guid>        </item>
        <item>
            <title>Gonadotropin-Releasing Hormone Inhibits Ether-a-Go-Go-Related Gene K+ Currents in Mouse Gonadotropes.</title>
            <link>http://www.medworm.com/index.php?rid=3173619&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20068004%26dopt%3DAbstract</link>
            <description>In conclusion, the erg current contributes to the maintenance of the resting potential in gonadotropes, thereby securing a low [Ca(2+)]i by restricting Ca(2+) influx. In addition, the erg channels are modulated by GnRH by an as-yet unknown signal cascade.
    PMID: 20068004 [PubMed - as supplied by publisher] (Source: Endocrinology)</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3173619</comments>
            <pubDate>Tue, 12 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3173619</guid>        </item>
        <item>
            <title>Transient Estradiol Exposure during Middle Age in Ovariectomized Rats Exerts Lasting Effects on Cognitive Function and the Hippocampus.</title>
            <link>http://www.medworm.com/index.php?rid=3173618&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20068005%26dopt%3DAbstract</link>
            <description>Authors: Rodgers SP, Bohacek J, Daniel JM
    We determined whether transient exposure to estradiol during middle age in ovariectomized rats would exert lasting effects on cognition and the brain beyond the period of exposure. Two experiments were conducted. Rats 10-11 months of age were ovariectomized and received vehicle control treatment throughout the experiment, continuous estradiol treatment throughout the experiment, or 40 d of transient exposure to estradiol that ended 3 d before behavioral training. In the first experiment, rats were trained on a radial-maze working memory task and killed 2 months after the termination of transient exposure to estradiol. The hippocampus was immunostained for choline acetyltransferase and estrogen receptors alpha (ERalpha) and beta (ERbeta) by West...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3173618</comments>
            <pubDate>Tue, 12 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3173618</guid>        </item>
        <item>
            <title>Moderate Caloric Restriction in Lactating Rats Protects Offspring against Obesity and Insulin Resistance in Later Life.</title>
            <link>http://www.medworm.com/index.php?rid=3173617&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20068006%26dopt%3DAbstract</link>
            <description>Authors: Palou M, Priego T, S&amp;#xE1;nchez J, Torrens JM, Palou A, Pic&amp;#xF3; C
    We aimed to assess the lasting effects of caloric restriction in lactating rats on body weight and insulin sensitivity of their offspring. Dams were fed with either ad libitum standard diet or a 30% caloric restricted diet throughout lactation. After weaning, the offspring were fed with a normal-fat diet until the age of 15 wk, and then with a normal- or a high-fat (HF) diet until the age of 26 wk. Blood parameters were measured during ad libitum feeding conditions and after 14-h fasting. Food preferences were also measured. In dams, milk leptin concentration and leptin mRNA and protein levels in mammary gland were also determined. Caloric restricted dams showed higher mRNA and protein levels of leptin in mamm...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3173617</comments>
            <pubDate>Tue, 12 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3173617</guid>        </item>
        <item>
            <title>Nonmuscle Myosin IIA (Myosin Heavy Polypeptide 9): A Novel Class of Signal Transducer Mediating the Activation of G{alpha}h/Phospholipase C-{delta}1 Pathway.</title>
            <link>http://www.medworm.com/index.php?rid=3173616&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20068007%26dopt%3DAbstract</link>
            <description>Authors: Lin YF, Yeh TS, Chen SF, Tsai YH, Chou CM, Yang YY, Huang HM
    The dimeric Gh protein is comprised of alpha (tissue transglutaminase) and beta (Calreticulin) subunits and known to be associated with FSH-, oxytocin-, or epinephrine-receptors/functions in their respective target cells. After establishing the FSH-induced activation of Galphah/phospholipase C (PLC)-delta1 pathway in rat Sertoli cells (SCs), we have attempted to identify a possible Galphah-coupled novel FSH receptor (FSH-R). Remarkably, a protein with approximately 240-kDa molecular mass was coimmunoprecipitated with Galphah in the fractionated membrane proteins of rat SCs. The protein was identified as myosin heavy polypeptide 9 (MyH9) by mass spectrometric analysis and immunoblotting. In addition, immunoprecipitati...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3173616</comments>
            <pubDate>Tue, 12 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3173616</guid>        </item>
        <item>
            <title>The Protein Kinase A Pathway-Regulated Transcriptome of Endometrial Stromal Fibroblasts Reveals Compromised Differentiation and Persistent Proliferative Potential in Endometriosis.</title>
            <link>http://www.medworm.com/index.php?rid=3173615&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20068008%26dopt%3DAbstract</link>
            <description>Authors: Aghajanova L, Horcajadas JA, Weeks JL, Esteban FJ, Nezhat CN, Conti M, Giudice LC
    Intrinsic abnormalities in transplanted eutopic endometrium are believed to contribute to the pathogenesis of pelvic endometriosis. Herein we investigated transcriptomic differences in human endometrial stromal fibroblasts (hESFs) from women with (hESFendo) vs. without (hESFnonendo) endometriosis, in response to activation of the protein kinase A (PKA) pathway with 8-bromoadenosine-cAMP (8-Br-cAMP). hESFnonendo (n = 4) and hESFendo (n = 4) were isolated from eutopic endometrium and treated +/- 0.5 mM 8-Br-cAMP for 96 h. Purified total RNA was subjected to microarray analysis using the whole-genome Gene 1.0 ST Affymetrix platform. A total of 691 genes were regulated in cAMP-treated hESFnonendo vs....</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3173615</comments>
            <pubDate>Tue, 12 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3173615</guid>        </item>
        <item>
            <title>Gene Expression Profiling Identifies Key Estradiol Targets in the Frontal Cortex of the Rat.</title>
            <link>http://www.medworm.com/index.php?rid=3173614&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20068009%26dopt%3DAbstract</link>
            <description>Authors: S&amp;#xE1;rv&amp;#xE1;ri M, Hrabovszky E, Kall&amp;#xF3; I, Galamb O, Solymosi N, Lik&amp;#xF3; I, Moln&amp;#xE1;r B, Tihanyi K, Szombathelyi Z, Liposits Z
    Estradiol modulates a wide range of neural functions in the frontal cerebral cortex where subsets of neurons express estrogen receptor-alpha and -beta. Through these receptors, estradiol contributes to the maintenance of normal operation of the frontal cortex. During the decline of gonadal hormones, the frequency of neurological and psychiatric disorders increases. To shed light on the etiology of disorders related to declining levels of estrogens, we studied the genomic responses to estradiol. Ovariectomized rats were treated with a sc injection of estradiol. Twenty-four hours later, samples from the frontal cortices were dissected, and thei...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3173614</comments>
            <pubDate>Tue, 12 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3173614</guid>        </item>
        <item>
            <title>Disruption of the Single Copy Gonadotropin-Releasing Hormone Receptor in Mice by Gene Trap: Severe Reduction of Reproductive Organs and Functions in Developing and Adult Mice.</title>
            <link>http://www.medworm.com/index.php?rid=3173613&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20068010%26dopt%3DAbstract</link>
            <description>Authors: Wu S, Wilson MD, Busby ER, Isaac ER, Sherwood NM
    Mutations in the GnRH receptor gene (GNRHR) can result in hypogonadotropic hypogonadism in humans. Unlike most mammals, mice lack a second form of GnRH (GnRH2) and a type 2 GnRH receptor. To determine whether the GnRH receptor is critical at all stages of reproduction and whether this receptor has additional physiological functions in developing and adult mice, we have generated mice from an embryonic stem cell line containing a retroviral vector with multiple stop codons inserted into intron 1 of the Gnrhr gene. This gene trap insertion resulted in the disruption of exon 2 and exon 3 of the Gnrhr gene. The insertion also contained a lacZ gene that was used as a reporter for GnRH receptor expression in these mice. This model has...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3173613</comments>
            <pubDate>Tue, 12 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3173613</guid>        </item>
        <item>
            <title>Sensitivity of Cardiac Carnitine Palmitoyltransferase to Malonyl-CoA Is Regulated by Leptin. Similarities with a Model of Endogenous Hyperleptinemia.</title>
            <link>http://www.medworm.com/index.php?rid=3160089&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20056820%26dopt%3DAbstract</link>
            <description>Authors: Guzm&amp;#xE1;n-Ruiz R, Somoza B, Gil-Ortega M, Merino B, Cano V, Attan&amp;#xE9; C, Castan-Laurell I, Valet P, Fern&amp;#xE1;ndez-Alfonso MS, Ruiz-Gayo M
    Acute leptin increase as well as endogenous hyperleptinemia evoked by high-fat diets (HF) activate fatty acid metabolism in nonadipose tissues. This supports the notion that hyperleptinemia is pivotal to prevent/delay steatosis during periods of positive energy balance. We have previously shown that long-term HF spares ectopic accumulation of lipids specifically in the miocardium. Because carnitine palmitoyltransferase I (CPT-I) allows mitochondrial uptake/oxidation of fatty acids, we have hypothesized that leptin drives cardiac CPT-I activity. In the current study, hyperleptinemia was induced in C57BL/6J mice either by exogenous leptin...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3160089</comments>
            <pubDate>Thu, 07 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3160089</guid>        </item>
        <item>
            <title>Effects of Bone Morphogenetic Protein (BMP) on Adrenocorticotropin Production by Pituitary Corticotrope Cells: Involvement of Up-Regulation of BMP Receptor Signaling by Somatostatin Analogs.</title>
            <link>http://www.medworm.com/index.php?rid=3160088&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20056821%26dopt%3DAbstract</link>
            <description>Authors: Tsukamoto N, Otsuka F, Miyoshi T, Yamanaka R, Inagaki K, Yamashita M, Otani H, Takeda M, Suzuki J, Ogura T, Iwasaki Y, Makino H
    The mechanism by which somatostatin analogs suppress ACTH production by corticotropinomas has yet to be fully elucidated. We here studied the effects of somatostatin analogs on ACTH secretion using mouse corticotrope AtT20 cells focusing on the biological activity of bone morphogenetic proteins (BMPs). BMP ligands, receptors and Smads, and somatostatin receptors (SSTRs)-2, -3, and -5 were expressed in AtT20 cells. BMP-2, -4, -6, and -7 decreased basal ACTH production with BMP-4 effects being the most prominent. BMP-4 also inhibited CRH-induced ACTH production and proopiomelanocortin (POMC) transcription. However, the decrease in CRH-induced cAMP accum...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3160088</comments>
            <pubDate>Thu, 07 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3160088</guid>        </item>
        <item>
            <title>Mice Lacking Hepatic Lipase Are Lean and Protected against Diet-Induced Obesity and Hepatic Steatosis.</title>
            <link>http://www.medworm.com/index.php?rid=3160087&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20056822%26dopt%3DAbstract</link>
            <description>Authors: Chiu HK, Qian K, Ogimoto K, Morton GJ, Wisse BE, Agrawal N, McDonald TO, Schwartz MW, Dichek HL
    Hepatic lipase (HL)-mediated lipoprotein hydrolysis provides free fatty acids for energy, storage, and nutrient signaling and may play a role in energy homeostasis. Because HL-activity increases with increased visceral fat, we hypothesized that increased HL-activity favors weight gain and obesity and consequently, that HL deficiency would reduce body fat stores and protect against diet-induced obesity. To test this hypothesis, we compared wild-type mice (with endogenous HL) and mice genetically deficient in HL with respect to daily body weight and food intake, body composition, and adipocyte size on both chow and high-fat (HF) diets. Key determinants of energy expenditure, including...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3160087</comments>
            <pubDate>Thu, 07 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3160087</guid>        </item>
        <item>
            <title>LEFTY, a Member of the Transforming Growth Factor-{beta} Superfamily, Inhibits Uterine Stromal Cell Differentiation: A Novel Autocrine Role.</title>
            <link>http://www.medworm.com/index.php?rid=3160086&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20056823%26dopt%3DAbstract</link>
            <description>Authors: Tang M, Naidu D, Hearing P, Handwerger S, Tabibzadeh S
    LEFTY is expressed in normal endometrium in cells that decidualize. To understand the importance of this expression, we have studied the effect of LEFTY on decidualization in vitro and in vivo. Exposure of human uterine fibroblast (HuF) cells to recombinant LEFTY blocked the induction of the decidual differentiation-specific marker genes, IGFBP1 (IGF-binding protein 1) and PRL (prolactin) in response to medroxyprogesterone acetate, estradiol, and prostaglandin E2. The inhibitory effect was associated with decreased induction of the transcription factors ETS1 and FOXO1, both of which are essential for decidualization. Overexpression of LEFTY in decidualized HuF cells with an adenovirus that transduced LEFTY caused a marked ...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3160086</comments>
            <pubDate>Thu, 07 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3160086</guid>        </item>
        <item>
            <title>Doublesex- and Mab-3-Related Transcription Factor-1 Repression of Aromatase Transcription, a Possible Mechanism Favoring the Male Pathway in Tilapia.</title>
            <link>http://www.medworm.com/index.php?rid=3160085&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20056824%26dopt%3DAbstract</link>
            <description>Authors: Wang DS, Zhou LY, Kobayashi T, Matsuda M, Shibata Y, Sakai F, Nagahama Y
    Doublesex and Mab-3-related transcription factor-1 (Dmrt1) is an important transcription factor implicated in early testicular differentiation in vertebrates, but its target genes are largely unknown. In the Nile tilapia, estrogen is the natural inducer of ovarian differentiation. Our recent studies have shown that Forkhead-l2 up-regulated transcription of the Cyp19a1a gene (aromatase) in the gonads in a female-specific manner. However, the upstream factor(s) down-regulating Cyp19a1a expression during testicular differentiation remains unclear. In the present study, we used in vitro (promoter analysis) and in vivo (transgenesis and in situ hybridization) approaches to examine whether Dmrt1 inhibits Cyp19a...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3160085</comments>
            <pubDate>Thu, 07 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3160085</guid>        </item>
        <item>
            <title>Precursor Cells in Mouse Islets Generate New {beta}-Cells in Vivo during Aging and after Islet Injury.</title>
            <link>http://www.medworm.com/index.php?rid=3160084&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20056825%26dopt%3DAbstract</link>
            <description>Authors: Liu H, Guz Y, Kedees MH, Winkler J, Teitelman G
    Whereas it is believed that the pancreatic duct contains endocrine precursors, the presence of insulin progenitor cells residing in islets remain controversial. We tested whether pancreatic islets of adult mice contain precursor beta-cells that initiate insulin synthesis during aging and after islet injury. We used bigenic mice in which the activation of an inducible form of Cre recombinase by a one-time pulse of tamoxifen results in the permanent expression of a floxed human placental alkaline phosphatase (PLAP) gene in 30% of pancreatic beta-cells. If islets contain PLAP(-) precursor cells that differentiate into beta-cells (PLAP(-)IN(+)), a decrease in the percentage of PLAP(+)IN(+) cells per total number of IN(+) cells would ...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3160084</comments>
            <pubDate>Thu, 07 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3160084</guid>        </item>
        <item>
            <title>Vinclozolin Exposure in Utero Induces Postpubertal Prostatitis and Reduces Sperm Production via a Reversible Hormone-Regulated Mechanism.</title>
            <link>http://www.medworm.com/index.php?rid=3160083&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20056826%26dopt%3DAbstract</link>
            <description>Authors: Cowin PA, Gold E, Aleksova J, O'Bryan MK, Foster PM, Scott HS, Risbridger GP
    Vinclozolin is an endocrine-disrupting chemical (EDC) that binds with high affinity to the androgen receptor (AR) and blocks the action of gonadal hormones on male reproductive organs. An alternative mechanism of action of Vinclozolin involves transgenerational effects on the male reproductive tract. We previously reported in utero Vinclozolin exposure-induced prostatitis (prostate inflammation) in postpubertal rats concurrent with down-regulation of AR and increased nuclear factor-kappaB activation. We postulated the male reproductive abnormalities induced by in utero Vinclozolin exposure could be reversed by testosterone supplementation, in contrast to the permanent modifications involving DNA methy...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3160083</comments>
            <pubDate>Thu, 07 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3160083</guid>        </item>
        <item>
            <title>Thyroid Hormone Regulation of Gene Expression in the Developing Rat Fetal Cerebral Cortex: Prominent Role of the Ca2+/Calmodulin-Dependent Protein Kinase IV Pathway.</title>
            <link>http://www.medworm.com/index.php?rid=3160082&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20056827%26dopt%3DAbstract</link>
            <description>Authors: Morte B, D&amp;#xED;ez D, Aus&amp;#xF3; E, Belinch&amp;#xF3;n MM, Gil-Ib&amp;#xE1;&amp;#xF1;ez P, Grijota-Mart&amp;#xED;nez C, Navarro D, Morreale de Escobar G, Berbel P, Bernal J
    Thyroid hormones influence brain development through regulation of gene expression mediated by nuclear receptors. Nuclear receptor concentration increases rapidly in the human fetus during the second trimester, a period of high sensitivity of the brain to thyroid hormones. In the rat, the equivalent period is the last quarter of pregnancy. However, little is known about thyroid hormone action in the fetal brain, and in rodents, most thyroid hormone-regulated genes have been identified during the postnatal period. To identify potential targets of thyroid hormone in the fetal brain, we induced maternal and fetal hypothyroidis...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3160082</comments>
            <pubDate>Thu, 07 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3160082</guid>        </item>
        <item>
            <title>An Increase in the Circulating Concentration of Monocyte Chemoattractant Protein-1 Elicits Systemic Insulin Resistance Irrespective of Adipose Tissue Inflammation in Mice.</title>
            <link>http://www.medworm.com/index.php?rid=3160081&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20056828%26dopt%3DAbstract</link>
            <description>Authors: Tateya S, Tamori Y, Kawaguchi T, Kanda H, Kasuga M
    Chronic inflammation in adipose tissue is thought to be important for the development of insulin resistance in obesity. Furthermore, the level of monocyte chemoattractant protein-1 (MCP-1) is increased not only in adipose tissue but also in the circulation in association with obesity. However, it has remained unclear to what extent the increased circulating level of MCP-1 contributes to insulin resistance. We have now examined the relevance of circulating MCP-1 to the development of insulin resistance in mice. The plasma concentration of MCP-1 was increased chronically or acutely in mice to the level observed in obese animals by chronic subcutaneous infusion of recombinant MCP-1 with an osmotic pump or by acute intravenous inf...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3160081</comments>
            <pubDate>Thu, 07 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3160081</guid>        </item>
        <item>
            <title>Growth Hormone Secretagogues Reduce Transient Outward K+ Current via Phospholipase C/Protein Kinase C Signaling Pathway in Rat Ventricular Myocytes.</title>
            <link>http://www.medworm.com/index.php?rid=3160080&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20056829%26dopt%3DAbstract</link>
            <description>Authors: Sun Q, Zang WJ, Chen C
    Endogenous ghrelin and its synthetic counterpart hexarelin are peptide GH secretagogues (GHS) that exert a positive ionotropic effect in the cardiovascular system. The mechanism by which GHS modulate cardiac electrophysiology properties to alter myocyte contraction is poorly understood. In the present study, we examined whether GHS regulates the transient outward potassium current (Ito) as well as the putative intracellular signaling cascade responsible for such regulation. GHS and experimental agents were applied locally onto freshly isolated adult Sprague-Dawley rat ventricular myocytes and action potential morphology and Ito was recorded using nystatin-perforated whole-cell patch-clamp recording technique. Under current clamp, ghrelin and hexarelin (1...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3160080</comments>
            <pubDate>Thu, 07 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3160080</guid>        </item>
        <item>
            <title>Effects of Estradiol on Cerebrospinal Fluid Levels of Agouti-Related Protein in Ovariectomized Rhesus Monkeys.</title>
            <link>http://www.medworm.com/index.php?rid=3160079&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20056830%26dopt%3DAbstract</link>
            <description>Authors: Xiao E, Kim AJ, Dutia R, Conwell I, Ferin M, Wardlaw SL
    Hypothalamic proopiomelanocortin (POMC)-derived MSH peptides and the melanocortin receptor antagonist, agouti-related protein (AgRP), interact to regulate energy balance. Both POMC and AgRP neurons express estrogen receptors, but little is known about estrogen regulation of the melanocortin system in the primate. We have therefore examined the effects of physiological doses of estradiol (E2) on POMC and AgRP in lumbar cerebrospinal fluid (CSF) of ovariectomized monkeys. POMC prohormone was measured by ELISA. AgRP was measured by RIA (sensitive for the more biologically active C-terminal AgRP83-132 but also detects full-length AgRP) and by ELISA (measures primarily full length AgRP). In the first experiment, 14 animals wer...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3160079</comments>
            <pubDate>Thu, 07 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3160079</guid>        </item>
        <item>
            <title>Kit Ligand and the Somatostatin Receptor Antagonist, BIM-23627, Stimulate in Vitro Resting Follicle Growth in the Neonatal Mouse Ovary.</title>
            <link>http://www.medworm.com/index.php?rid=3160078&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20056831%26dopt%3DAbstract</link>
            <description>In conclusion, extraovarian SST, acting through its receptors 2 and 5 present on granulosa cells, may be involved in mouse folliculogenesis by reducing recruitment of resting follicles.
    PMID: 20056831 [PubMed - as supplied by publisher] (Source: Endocrinology)</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3160078</comments>
            <pubDate>Thu, 07 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3160078</guid>        </item>
        <item>
            <title>Acute Insulin Signaling in Pancreatic Beta-Cells Is Mediated by Multiple Raf-1 Dependent Pathways.</title>
            <link>http://www.medworm.com/index.php?rid=3160077&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20056832%26dopt%3DAbstract</link>
            <description>Authors: Alejandro EU, Kalynyak TB, Taghizadeh F, Gwiazda KS, Rawstron EK, Jacob KJ, Johnson JD
    Insulin enhances the proliferation and survival of pancreatic beta-cells, but its mechanisms remain unclear. We hypothesized that Raf-1, a kinase upstream of both ERK and Bad, might be a critical target of insulin in beta-cells. To test this hypothesis, we treated human and mouse islets as well as MIN6 beta-cells with multiple insulin concentrations and examined putative downstream targets using immunoblotting, immunoprecipitation, quantitative fluorescent imaging, and cell death assays. Low doses of insulin rapidly activated Raf-1 by dephosphorylating serine 259 and phosphorylating serine 338 in human islets, mouse islets, and MIN6 cells. The phosphorylation of ERK by insulin was eliminated...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3160077</comments>
            <pubDate>Thu, 07 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3160077</guid>        </item>
        <item>
            <title>17{beta}-Estradiol Accelerates Tumor Onset and Decreases Survival in a Transgenic Mouse Model of Ovarian Cancer.</title>
            <link>http://www.medworm.com/index.php?rid=3160076&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20056833%26dopt%3DAbstract</link>
            <description>Authors: Laviolette LA, Garson K, Macdonald EA, Senterman MK, Courville K, Crane CA, Vanderhyden BC
    Epithelial ovarian cancer is thought to be derived from the ovarian surface epithelium (OSE) but often goes undetected in the early stages, and as a result, the factors that contribute to its initiation and progression remain poorly understood. Epidemiological studies have suggested that the female steroid hormones are involved in ovarian carcinogenesis and that women who use hormone replacement therapy are at increased risk of developing the disease. A novel transgenic mouse model of ovarian cancer (tgCAG-LS-TAg) was developed to examine the role of the female reproductive steroid hormones [17beta-estradiol (E2) and progesterone (P4)] on the initiation, progression, and pathology of ova...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3160076</comments>
            <pubDate>Thu, 07 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3160076</guid>        </item>
        <item>
            <title>Effects of Estradiol on the Thermoneutral Zone and Core Temperature in Ovariectomized Rats.</title>
            <link>http://www.medworm.com/index.php?rid=3149724&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20051485%26dopt%3DAbstract</link>
            <description>Authors: Dacks PA, Rance NE
    Hot flushes represent a disorder of central thermoregulation characterized by the episodic activation of heat loss mechanisms. Although flushes are associated with estrogen withdrawal, there is little understanding of the effects of estrogen on thermoregulation in any species. It has been proposed that hormone withdrawal increases the sensitivity of hypothalamic neural pathways that control heat dissipation effectors. If so, we predicted that ovariectomized rats without estradiol treatment would activate tail skin vasodilatation (a major heat loss effector) at lower ambient temperatures and thereby lower the thermoneutral zone. The thermoneutral zone, defined as the range of ambient temperatures in which thermoregulation is achieved only by sensible (dry) he...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3149724</comments>
            <pubDate>Tue, 05 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3149724</guid>        </item>
        <item>
            <title>Pregnancy Up-Regulates Intestinal Calcium Absorption and Skeletal Mineralization Independently of the Vitamin D Receptor.</title>
            <link>http://www.medworm.com/index.php?rid=3149723&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20051486%26dopt%3DAbstract</link>
            <description>Authors: Fudge NJ, Kovacs CS
    Without the vitamin D receptor (VDR), adult mammals develop reduced intestinal calcium absorption, rickets, and osteomalacia. Intestinal calcium absorption normally increases during pregnancy so that the mother can supply sufficient calcium to her fetuses. The maternal skeleton is rapidly resorbed during lactation to provide calcium needed for milk; that lost bone mineral content (BMC) is completely restored after weaning. We studied Vdr null mice to determine whether these adaptations during pregnancy and lactation require the VDR. Vdr nulls were severely rachitic at 10 wk of age on a normal diet. Pregnancy induced a 158% increase in Vdr null BMC to equal the pregnant wild-type (WT) value. Lactation caused BMC losses that were equal in Vdr nulls and WT. Vd...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3149723</comments>
            <pubDate>Tue, 05 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3149723</guid>        </item>
        <item>
            <title>RFamide-Related Peptide and Messenger Ribonucleic Acid Expression in Mammalian Testis: Association with the Spermatogenic Cycle.</title>
            <link>http://www.medworm.com/index.php?rid=3149722&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20051487%26dopt%3DAbstract</link>
            <description>Authors: Zhao S, Zhu E, Yang C, Bentley GE, Tsutsui K, Kriegsfeld LJ
    RFamide-related peptide (RFRP), the mammalian homolog of avian gonadotropin-inhibitory hormone, has a pronounced suppressive action on the reproductive axis across species. In mammals, RFRP acts directly on GnRH neurons, and likely at the level of the pituitary, to inhibit gonadotropin secretion. In the present study, we examined whether RFRP might act outside of mammalian brain on reproductive tissues directly. Using RT-PCR and in situ hybridization, we found that both RFRP and its receptors [G protein-coupled receptor (GPR) 147 and GPR74] are expressed in the testis of Syrian hamster. These results were confirmed and extended using double- and triple-label immunohistochemistry. RFRP expression was observed in sperma...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3149722</comments>
            <pubDate>Tue, 05 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3149722</guid>        </item>
        <item>
            <title>Gonadotropin-Releasing Hormone-I-Mediated Activation of Progesterone Receptor Contributes to Gonadotropin {alpha}-Subunit Expression in Mouse Gonadotrophs.</title>
            <link>http://www.medworm.com/index.php?rid=3149721&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20051488%26dopt%3DAbstract</link>
            <description>Authors: Chen J, An BS, So WK, Cheng L, Hammond GL, Leung PC
    In pituitary cells, cross talk between GnRH-I and the progesterone receptor accentuates gonadotropin production. We show that GnRH-I activates a progesterone response element (PRE)-driven luciferase reporter gene at 8 h and gonadotropin alpha-subunit (gsualpha) gene expression at 24 h in two mouse gonadotrope cell lines, alphaT3-1 and LbetaT2. In alphaT3-1 cells, progesterone had an additive effect on GnRH-I-induced PRE-luciferase reporter gene activity but not on GSUalpha mRNA levels. However, progesterone had no synergistic effect on the GnRH-I-induced expression of these genes in LbetaT2 cells. Up-regulation of the PRE-luciferase reporter gene by GnRH-I was attenuated by pretreatment with protein kinase A (H89) and protein...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3149721</comments>
            <pubDate>Tue, 05 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3149721</guid>        </item>
        <item>
            <title>Differential Release of Matrix Metalloproteinases and Tissue Inhibitors of Metalloproteinases by Human Granulosa-Lutein Cells and Ovarian Leukocytes.</title>
            <link>http://www.medworm.com/index.php?rid=3149720&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20051489%26dopt%3DAbstract</link>
            <description>In this study we investigated the cellular source of ovarian MMPs and TIMPs. Cells isolated from the preovulatory human follicle were cultured after immunobead depletion of CD45-expressing cells, which allowed differential assessment of leukocyte and granulosa-lutein cell fractions. Secretion of MMP-9 by follicular fluid-derived cells was associated with the presence of leukocytes. Granulosa-lutein cells synthesized low levels of MMP-9 but failed to secrete this enzyme that presumably accumulated in the cytoplasm, indicated by an increased MMP-9 expression of luteinized cells in sectioned midluteal phase corpora lutea. Synthesis and secretion of TIMP by follicular fluid-derived cells was associated with granulosa-lutein cells. TIMPs derived by granulosa-lutein cells failed to inhibit MMP-r...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3149720</comments>
            <pubDate>Tue, 05 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3149720</guid>        </item>
        <item>
            <title>The Nuclear Receptor Corepressor Has Organizational Effects within the Developing Amygdala on Juvenile Social Play and Anxiety-Like Behavior.</title>
            <link>http://www.medworm.com/index.php?rid=3149719&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20051490%26dopt%3DAbstract</link>
            <description>Authors: Jessen HM, Kolodkin MH, Bychowski ME, Auger CJ, Auger AP
    Nuclear receptor function on DNA is regulated by the balanced recruitment of coregulatory complexes. Recruited proteins that increase gene expression are called coactivators, and those that decrease gene expression are called corepressors. Little is known about the role of corepressors, such as nuclear receptor corepressor (NCoR), on the organization of behavior. We used real-time PCR to show that NCoR mRNA levels are sexually dimorphic, that females express higher levels of NCoR mRNA within the developing amygdala and hypothalamus, and that NCoR mRNA levels are reduced by estradiol treatment. To investigate the functional role of NCoR on juvenile social behavior, we infused small interfering RNA targeted against NCoR wi...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3149719</comments>
            <pubDate>Tue, 05 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3149719</guid>        </item>
        <item>
            <title>Fraud: just say no!</title>
            <link>http://www.medworm.com/index.php?rid=3120940&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20028876%26dopt%3DAbstract</link>
            <description>Authors: Blaustein JD
    
    PMID: 20028876 [PubMed - in process] (Source: Endocrinology)</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3120940</comments>
            <pubDate>Sat, 26 Dec 2009 04:14:51 +0100</pubDate>
            <guid isPermaLink="false">3120940</guid>        </item>
        <item>
            <title>Fat and energy economy in hypo- and hyperthyroidism are not the mirror image of one another.</title>
            <link>http://www.medworm.com/index.php?rid=3120939&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20028877%26dopt%3DAbstract</link>
            <description>Authors: Silva JE
    
    PMID: 20028877 [PubMed - in process] (Source: Endocrinology)</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3120939</comments>
            <pubDate>Sat, 26 Dec 2009 04:14:49 +0100</pubDate>
            <guid isPermaLink="false">3120939</guid>        </item>
        <item>
            <title>The Follistatin-288 Isoform Alone Is Sufficient for Survival But Not for Normal Fertility in Mice.</title>
            <link>http://www.medworm.com/index.php?rid=3120938&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20032047%26dopt%3DAbstract</link>
            <description>Authors: Kimura F, Sidis Y, Bonomi L, Xia Y, Schneyer A
    Follistatin (FST) is a natural antagonist of activin and related TGFbeta superfamily ligands that exists as three protein isoforms differing in length at the C terminus. The longest FST315 isoform is found in the circulation, whereas the shortest FST288 isoform is typically found in or on cells and tissues, and the intermediate FST303 isoform is found in gonads. We recently demonstrated that the FST isoforms have distinct biological actions in vitro that, taken together with the differential distribution, suggests they may also have different roles in vivo. To explore the specific role of individual FST isoforms, we created a single-isoform FST288-only mouse. In contrast to the neonatal death of FST global knockout mice, FST288-on...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3120938</comments>
            <pubDate>Wed, 23 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3120938</guid>        </item>
        <item>
            <title>Minireview: The Play of Proteins on the Parathyroid Hormone Messenger Ribonucleic Acid Regulates Its Expression.</title>
            <link>http://www.medworm.com/index.php?rid=3120937&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20032048%26dopt%3DAbstract</link>
            <description>Authors: Naveh-Many T
    PTH regulates serum calcium and phosphate levels and bone strength. The parathyroid is unique in that the trigger for PTH secretion is a low extracellular calcium rather than high calcium as for other hormones. The parathyroid senses small changes in serum calcium through the seven-trans-membrane G protein-coupled calcium receptor to alter PTH secretion. PTH then acts on bone and kidney to correct serum calcium. Parathyroid cells have few secretory granules as compared with other endocrine cells, and therefore PTH production is regulated largely at the levels of PTH gene expression and parathyroid cell proliferation. The regulation of PTH gene expression by changes in calcium and phosphate and in chronic kidney failure is posttranscriptional involving the binding ...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3120937</comments>
            <pubDate>Wed, 23 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3120937</guid>        </item>
        <item>
            <title>Minireview: Posttranscriptional Regulation of the Insulin and Insulin-Like Growth Factor Systems.</title>
            <link>http://www.medworm.com/index.php?rid=3120936&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20032049%26dopt%3DAbstract</link>
            <description>Authors: Lee EK, Gorospe M
    Insulin and IGFs share structural similarities and regulate metabolic processes including glucose homeostasis. Acute alterations in glucose levels trigger rapid changes in insulin concentration and insulin signaling. These processes are tightly regulated by posttranscriptional mechanisms that alter the stability and translation of mRNAs encoding insulin and the insulin receptor. Long-term glucose homeostasis is also modulated by IGFs and IGF receptors, whose expression is likewise subject to changes in the stability and translation of the encoding mRNAs. The control of mRNA half-life and translation is governed by RNA-binding proteins and microRNAs that interact with target transcripts at the 3' and 5' untranslated regions. In this review, we describe the RNA...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3120936</comments>
            <pubDate>Wed, 23 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3120936</guid>        </item>
        <item>
            <title>Corticotropin-Releasing Hormone Receptor-1 in Cerebral Microvessels Changes during Development and Influences Urocortin Transport across the Blood-Brain Barrier.</title>
            <link>http://www.medworm.com/index.php?rid=3120935&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20032050%26dopt%3DAbstract</link>
            <description>In this study we tested the hypothesis that receptor-mediated transport of urocortin across the blood-brain barrier (BBB) undergoes developmental changes. Urocortin is a peptide produced by both selective brain regions and peripheral organs, and it is involved in feeding, memory, mood, cardiovascular functions, and immune regulation. In BBB studies with multiple-time regression analysis, we found that neonatal mice had a significant influx of (125)I-urocortin. By contrast, adult mice did not transport urocortin across the BBB. Quantitative RT-PCR showed that corticotropin-releasing hormone receptor (CRHR)-1 was developmentally regulated in enriched cerebral microvessels as well as hypothalamus, being significantly higher in neonatal than adult mice. This change was less dramatic in agouti ...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3120935</comments>
            <pubDate>Wed, 23 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3120935</guid>        </item>
        <item>
            <title>The Thyrotropin-Releasing Hormone Gene Is Regulated by Thyroid Hormone at the Level of Transcription in Vivo.</title>
            <link>http://www.medworm.com/index.php?rid=3120934&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20032051%26dopt%3DAbstract</link>
            <description>Authors: Sugrue ML, Vella KR, Morales C, Lopez ME, Hollenberg AN
    The expression of the TRH gene in the paraventricular nucleus (PVH) of the hypothalamus is required for the normal production of thyroid hormone (TH) in rodents and humans. In addition, the regulation of TRH mRNA expression by TH, specifically in the PVH, ensures tight control of the set point of the hypothalamic-pituitary-thyroid axis. Although many studies have assumed that the regulation of TRH expression by TH is at the level of transcription, there is little data available to demonstrate this. We used two in vivo model systems to show this. In the first model system, we developed an in situ hybridization (ISH) assay directed against TRH heteronuclear RNA to measure TRH transcription directly in vivo. We show that in ...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3120934</comments>
            <pubDate>Wed, 23 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3120934</guid>        </item>
        <item>
            <title>Prolactin Exerts a Prosurvival Effect on Human Spermatozoa via Mechanisms that Involve the Stimulation of Akt Phosphorylation and Suppression of Caspase Activation and Capacitation.</title>
            <link>http://www.medworm.com/index.php?rid=3120933&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20032052%26dopt%3DAbstract</link>
            <description>Authors: Pujianto DA, Curry BJ, Aitken RJ
    The purpose of this study was to examine the impact of prolactin (PRL) on human sperm function, in light of a recent proteomic analysis indicating that these cells express the PRL receptor (PRLR). Immunocytochemical analyses confirmed the presence of PRLR in human spermatozoa and localized this receptor to the postacrosomal region of the sperm head as well as the neck, midpiece, and principal piece of the sperm tail. Nested PCR analysis indicated that these cells possess four splice variants of the PRLR: the long form and three short isoforms, one of which is reported for the first time. A combination of Western blot analyses and immunocytochemistry demonstrated that PRL inhibited sperm capacitation in a dose-dependent manner, suppressing SRC k...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3120933</comments>
            <pubDate>Wed, 23 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3120933</guid>        </item>
        <item>
            <title>Inhibitor of Differentiation (Id) Genes Are Expressed in the Steroidogenic Cells of the Ovine Ovary and Are Differentially Regulated by Members of the Transforming Growth Factor-{beta} Family.</title>
            <link>http://www.medworm.com/index.php?rid=3120932&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20032053%26dopt%3DAbstract</link>
            <description>Authors: Hogg K, Etherington SL, Young JM, McNeilly AS, Duncan WC
    Inhibitor of differentiation (Id) proteins act during embryogenesis and development to repress gene transcription required for lineage commitment, while promoting cell growth. Growth factors belonging to the TGFbeta superfamily of signaling molecules, notably the bone morphogenetic proteins (BMPs) and activin, can regulate Id expression in these tissues. Id expression and function in adult physiology is less well determined, and we hypothesized a role for Id proteins in the adult mammalian ovary. Immunohistochemistry for Id1, Id2, Id3, and Id4 in the sheep ovary revealed consistent expression in granulosa and thecal cells of ovarian follicles throughout development. In atretic follicles, Id proteins were selectively down...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3120932</comments>
            <pubDate>Wed, 23 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3120932</guid>        </item>
        <item>
            <title>Regular Pacemaker Activity Characterizes Gonadotropin-Releasing Hormone 2 Neurons Recorded from Green Fluorescent Protein-Transgenic Medaka.</title>
            <link>http://www.medworm.com/index.php?rid=3120931&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20032054%26dopt%3DAbstract</link>
            <description>Authors: Kanda S, Nishikawa K, Karigo T, Okubo K, Isomae S, Abe H, Kobayashi D, Oka Y
    GnRH2 is a molecule conserved from fish to humans, suggesting its important functions. However, recent studies have shown that GnRH2 neurons project widely in the brain but not to the pituitary, which suggests their functions other than stimulation of gonadotropin secretion. In contrast to the wealth of knowledge in GnRH1 and GnRH3 neuronal systems, the GnRH2 neuronal system remains to be studied, and there has been no single cell approach so far, partly because of the lack of GnRH2 system in rodents. Here, we generated GnRH2-green fluorescent protein (GFP) transgenic medaka for the first single cell electrophysiological recording from GnRH2 neurons in vertebrates. Whole-cell and on-cell patch clamp a...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3120931</comments>
            <pubDate>Wed, 23 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3120931</guid>        </item>
        <item>
            <title>Antidiabetic Properties of Zinc-{alpha}2-Glycoprotein in ob/ob Mice.</title>
            <link>http://www.medworm.com/index.php?rid=3120930&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20032055%26dopt%3DAbstract</link>
            <description>Authors: Russell ST, Tisdale MJ
    Zinc-alpha2-glycoprotein (ZAG) is an adipokine associated with fat loss in cancer cachexia. The purpose of this study was to evaluate the ability of recombinant human ZAG to attenuate type 2 diabetes in the ob/ob mouse model. ZAG (50 mug daily, iv) induced a progressive loss of body weight (3.5g in 5 d), without an effect on food or water intake but with a 0.4 C rise in body temperature, suggesting an increased energy expenditure. Despite an increased plasma glycerol, indicative of increased lipolysis, levels of glucose, triglycerides, and nonesterified fatty acids were decreased by 17, 25, and 62%, respectively, due to an increased use of both glucose and lipids by muscle and brown adipose tissue. The weight of the latter increased 2-fold, and there was...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3120930</comments>
            <pubDate>Wed, 23 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3120930</guid>        </item>
        <item>
            <title>Insulin-Like Growth Factor 2 and the Insulin Receptor, But Not Insulin, Regulate Fetal Hepatic Glycogen Synthesis.</title>
            <link>http://www.medworm.com/index.php?rid=3120929&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20032056%26dopt%3DAbstract</link>
            <description>In this study, we used several knockout mouse strains, including those lacking Pdx-1 (pancreatic duodenal homeobox-1), Insr (insulin receptor), and Igf2 (IGF-II) to determine the role of these genes in the regulation of fetal hepatic glycogen synthesis. Our data show that insulin deficiency does not alter hepatic glycogen stores, whereas Insr and Igf2 deficiency do. We found that both insulin receptor isoforms (IR-A and IR-B) are present in the fetal liver, and their expression is gestationally regulated. IR-B is highly expressed in the fetal liver; nonetheless, the percentage of hepatic IR-A isoform, which binds Igf2, was significantly higher in the fetus than the adult. In vitro experiments demonstrate that Igf2 increases phosphorylation of hepatic Insr, insulin receptor substrate-2, and...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3120929</comments>
            <pubDate>Wed, 23 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3120929</guid>        </item>
        <item>
            <title>Maternally Expressed Gene 3 (MEG3) Noncoding Ribonucleic Acid: Isoform Structure, Expression, and Functions.</title>
            <link>http://www.medworm.com/index.php?rid=3120928&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20032057%26dopt%3DAbstract</link>
            <description>This study establishes for the first time the structure-function relationship of a large noncoding RNA and provides a first look into the molecular mechanisms of the biological functions of a large noncoding RNA.
    PMID: 20032057 [PubMed - as supplied by publisher] (Source: Endocrinology)</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3120928</comments>
            <pubDate>Wed, 23 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3120928</guid>        </item>
        <item>
            <title>REDD1 Is a Major Target of Testosterone Action in Preventing Dexamethasone-Induced Muscle Loss.</title>
            <link>http://www.medworm.com/index.php?rid=3120927&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20032058%26dopt%3DAbstract</link>
            <description>Authors: Wu Y, Zhao W, Zhao J, Zhang Y, Qin W, Pan J, Bauman WA, Blitzer RD, Cardozo C
    Glucocorticoids are a well-recognized and common cause of muscle atrophy that can be prevented by testosterone. However, the molecular mechanisms underlying such protection have not been described. Thus, the global effects of testosterone on dexamethasone-induced changes in gene expression were evaluated in rat gastrocnemius muscle using DNA microarrays. Gene expression was analyzed after 7-d administration of dexamethasone, dexamethasone plus testosterone, or vehicle. Dexamethasone changed expression of 876 probe sets by at least 2-fold. Among these, 474 probe sets were changed by at least 2-fold in the opposite direction in the dexamethasone plus testosterone group (genes in opposition). Major biol...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3120927</comments>
            <pubDate>Wed, 23 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3120927</guid>        </item>
        <item>
            <title>Thyroid Hormone-Induced Cardiac Mechano Growth Factor Expression Depends on Beating Activity.</title>
            <link>http://www.medworm.com/index.php?rid=3120926&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20032059%26dopt%3DAbstract</link>
            <description>Authors: van Dijk-Ottens M, Vos IH, Cornelissen PW, de Bruin A, Everts ME
    The mechano growth factor (MGF), a splice variant of the IGF-I gene, was first discovered in mechanically overloaded skeletal muscle and was shown to play an important role in proliferation of muscle stem cells. Since then, the presence and effects of MGF have been demonstrated in other tissues. MGF has been shown to act neuroprotectively during brain ischemia, and pretreatment with MGF before myocardial infarction improves cardiac function. Because MGF plays a permissive role in exercise-induced skeletal muscle hypertrophy, we hypothesize that MGF is commonly involved in cardiac hypertrophy. To investigate the regulation of MGF expression in heart, mice were treated with thyroid hormone (T3) for 12 d to induce p...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3120926</comments>
            <pubDate>Wed, 23 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3120926</guid>        </item>
        <item>
            <title>Minireview: Delivering the Code: Polyplex Carriers for Deoxyribonucleic Acid and Ribonucleic Acid Interference Therapies.</title>
            <link>http://www.medworm.com/index.php?rid=3120925&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20032060%26dopt%3DAbstract</link>
            <description>Authors: Christie RJ, Nishiyama N, Kataoka K
    Nucleic acid-based therapies offer great potential for treatment of a variety of diseases including cancer by modulating protein expression with DNA or small interfering RNA. However, realization of their full therapeutic potential is currently limited due to an inability to reach the target site in an active form. Identification of delivery barriers such as stability in circulation, resistance to degradation and entrapment in subcellular vesicles has led to development of sophisticated multifunctional synthetic polymers for forming ionic complexes with nucleic acids and also providing performance-enhancing features. The most promising designs comprise features to help increase stability in circulation and also contain functionality to aid i...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3120925</comments>
            <pubDate>Wed, 23 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3120925</guid>        </item>
        <item>
            <title>Testosterone Induces Redistribution of Forkhead Box-3a and Down-Regulation of Growth and Differentiation Factor 9 Messenger Ribonucleic Acid Expression at Early Stage of Mouse Folliculogenesis.</title>
            <link>http://www.medworm.com/index.php?rid=3120924&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20032061%26dopt%3DAbstract</link>
            <description>Authors: Yang JL, Zhang CP, Li L, Huang L, Ji SY, Lu CL, Fan CH, Cai H, Ren Y, Hu ZY, Gao F, Liu YX
    Increasing evidence has shown that excess androgen may be a main cause of polycystic ovary syndrome (PCOS). However, the molecular mechanism of androgen action on the ovary is unclear. To investigate the possible impacts of androgen on early follicular development, neonatal mouse ovaries mainly containing primordial follicles were cultured with testosterone. We demonstrated that the number of primary follicles was increased after 10 d culture with testosterone treatment via phosphatidylinositol 3-kinase/Akt pathway. Androgen induced Forkhead box (Foxo)-3a activation, and translocation of Foxo3a protein from oocyte nuclei to cytoplasm, which might be a key step for primordial follicle act...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3120924</comments>
            <pubDate>Wed, 23 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3120924</guid>        </item>
        <item>
            <title>Testosterone Supplementation Reverses Sarcopenia in Aging through Regulation of Myostatin, c-Jun NH2-Terminal Kinase, Notch, and Akt Signaling Pathways.</title>
            <link>http://www.medworm.com/index.php?rid=3108805&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20022929%26dopt%3DAbstract</link>
            <description>Authors: Kovacheva EL, Sinha Hikim AP, Shen R, Sinha I, Sinha-Hikim I
    Aging in rodents and humans is characterized by loss of muscle mass (sarcopenia). Testosterone supplementation increases muscle mass in healthy older men. Here, using a mouse model, we investigated the molecular mechanisms by which testosterone prevents sarcopenia and promotes muscle growth in aging. Aged mice of 22 months of age received a single sc injection of GnRH antagonist every 2 wk to suppress endogenous testosterone production and were implanted subdermally under anesthesia with 0.5 or 1.0 cm testosterone-filled implants for 2 months (n = 15/group). Young and old mice (n = 15/group), of 2 and 22 months of age, respectively, received empty implants and were used as controls. Compared with young animals, a sig...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3108805</comments>
            <pubDate>Fri, 18 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3108805</guid>        </item>
        <item>
            <title>Endoplasmic Reticulum Stress-Induced Activation of Activating Transcription Factor 6 Decreases cAMP-Stimulated Hepatic Gluconeogenesis via Inhibition of CREB.</title>
            <link>http://www.medworm.com/index.php?rid=3108804&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20022930%26dopt%3DAbstract</link>
            <description>Authors: Seo HY, Kim MK, Min AK, Kim HS, Ryu SY, Kim NK, Lee KM, Kim HJ, Choi HS, Lee KU, Park KG, Lee IK
    The expression of genes encoding key hepatic gluconeogenic enzymes, including phosphoenolpyruvate carboxykinase (PEPCK) and glucose-6-phosphatase (G6Pase), is regulated at the transcriptional level by a network of transcription factors and cofactors, including cAMP response element-binding protein (CREB). It has been suggested that increased endoplasmic reticulum (ER) stress in the liver impairs hepatic glucose metabolism. However, the direct effect of ER stress on hepatic gluconeogenesis is still not clear. Here, we investigated whether ER stress influences hepatic gluconeogenesis and whether this process is mediated by activating transcription factor 6 (ATF6) through the inhibiti...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3108804</comments>
            <pubDate>Fri, 18 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3108804</guid>        </item>
        <item>
            <title>Role of Asparagine-Linked Glycosylation in Cell Surface Expression and Function of the Human Adrenocorticotropin Receptor (Melanocortin 2 Receptor) in 293/FRT Cells.</title>
            <link>http://www.medworm.com/index.php?rid=3108803&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20022931%26dopt%3DAbstract</link>
            <description>The objective of the present study is to examine whether N-glycosylation is essential or not for cell surface expression and cAMP production in native and MC2R accessory protein (MRAPalpha, -beta, or -dCT)-expressing cells using 293/FRT transfected with Myc-MC2R. Western blot analyses performed with or without endoglycosidase H, peptide:N-glycosidase F or tunicamycin treatments and site-directed mutagenesis revealed that MC2R was glycosylated in the N-terminal domain at its two putative N-glycosylation sites (Asn(12)-Asn(13)-Thr(14) and Asn(17)-Asn(18)-Ser(19)). In the absence of human MRAP coexpression, N-glycosylation of at least one of the two sites was necessary for MC2R cell surface expression. However, when MRAP was present, cell surface expression of MC2R mutants was either rescued ...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3108803</comments>
            <pubDate>Fri, 18 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3108803</guid>        </item>
        <item>
            <title>Cyclooxygenase 2 Inhibition Exacerbates Palmitate-Induced Inflammation and Insulin Resistance in Skeletal Muscle Cells.</title>
            <link>http://www.medworm.com/index.php?rid=3108802&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20022932%26dopt%3DAbstract</link>
            <description>Authors: Coll T, Palomer X, Blanco-Vaca F, Escol&amp;#xE0;-Gil JC, S&amp;#xE1;nchez RM, Laguna JC, V&amp;#xE1;zquez-Carrera M
    Palmitate-induced inflammation is involved in the development of insulin resistance in skeletal muscle cells. Here we evaluated the effect of the saturated fatty acid palmitate and the monounsaturated fatty acid oleate on Toll-like receptors (TLR)-2 and -4 and cyclooxygenase 2 (COX-2) expression and examined whether the inhibition of this enzyme modulates fatty acid-induced inflammation. Skeletal muscle cells exposed to palmitate showed enhanced TLR-2 and COX-2 mRNA levels, whereas oleate did not modify their expression. Palmitate-induced expression of these genes was dependent on nuclear factor (NF)-kappaB activation, because expression was reduced in the presence of the N...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3108802</comments>
            <pubDate>Fri, 18 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3108802</guid>        </item>
        <item>
            <title>Plasma Transcortin Influences Endocrine and Behavioral Stress Responses in Mice.</title>
            <link>http://www.medworm.com/index.php?rid=3108801&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20022933%26dopt%3DAbstract</link>
            <description>Authors: Richard EM, Helbling JC, Tridon C, Desmedt A, Minni AM, Cador M, Pourtau L, Konsman JP, Morm&amp;#xE8;de P, Moisan MP
    Glucocorticoids are released after hypothalamus-pituitary-adrenal axis stimulation by stress and act both in the periphery and in the brain to bring about adaptive responses that are essential for life. Dysregulation of the stress response can precipitate psychiatric diseases, in particular depression. Recent genetic studies have suggested that the glucocorticoid carrier transcortin, also called corticosteroid-binding globulin (CBG), may have an important role in stress response. We have investigated the effect of partial or total transcortin deficiency using transcortin knockout mice on hypothalamus-pituitary-adrenal axis functioning and regulation as well as on b...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3108801</comments>
            <pubDate>Fri, 18 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3108801</guid>        </item>
        <item>
            <title>Functional Role of c-Jun-N-Terminal Kinase in Feeding Regulation.</title>
            <link>http://www.medworm.com/index.php?rid=3108800&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20022934%26dopt%3DAbstract</link>
            <description>In this study, we show that central inhibition of JNK activity potentiates the stimulatory effects of glucocorticoids on food intake and that this effect is abolished in mice whose agouti-related peptide (AgRP) neurons are degenerated. JNK1-deficient mice feed more upon central administration of glucocorticoids, and glucocorticoid receptor nuclear immunoreactivity is enhanced in the AgRP neurons. JNK inhibition in hypothalamic explants stimulates Agrp expression, and JNK1-deficient mice exhibit increased Agrp expression, heightened hyperphagia, and weight gain during refeeding. Our study shows that JNK1 is a novel regulator of feeding by antagonizing glucocorticoid function in AgRP neurons. Paradoxically, JNK1 mutant mice feed less and lose more weight upon central administration of insuli...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3108800</comments>
            <pubDate>Fri, 18 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3108800</guid>        </item>
        <item>
            <title>Arcuate Nucleus Proopiomelanocortin Neurons Mediate the Acute Anorectic Actions of Leukemia Inhibitory Factor via gp130.</title>
            <link>http://www.medworm.com/index.php?rid=3101233&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20016025%26dopt%3DAbstract</link>
            <description>Authors: Grossberg AJ, Scarlett JM, Zhu X, Bowe DD, Batra AK, Braun TP, Marks DL
    The proinflammatory cytokine leukemia inhibitory factor (LIF) is induced in disease states and is known to inhibit food intake when administered centrally. However, the neural pathways underlying this effect are not well understood. We demonstrate that LIF acutely inhibits food intake by directly activating pro-opiomelanocortin (POMC) neurons in the arcuate nucleus of the hypothalamus. We show that arcuate POMC neurons express the LIF-R, and that LIF stimulates the release of the anorexigenic peptide, alpha-MSH from ex vivo hypothalami. Transgenic mice lacking gp130, the signal transducing subunit of the LIF-R complex, specifically in POMC neurons fail to respond to LIF. Furthermore, LIF does not stimulate...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3101233</comments>
            <pubDate>Wed, 16 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3101233</guid>        </item>
        <item>
            <title>Minireview: Nanoparticles and the Immune System.</title>
            <link>http://www.medworm.com/index.php?rid=3101232&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20016026%26dopt%3DAbstract</link>
            <description>Authors: Zolnik BS, Gonz&amp;#xE1;lez-Fern&amp;#xE1;ndez A, Sadrieh N, Dobrovolskaia MA
    Today nanotechnology is finding growing applications in industry, biology, and medicine. The clear benefits of using nanosized products in various biological and medical applications are often challenged by concerns about the lack of adequate data regarding their toxicity. One area of interest involves the interactions between nanoparticles and the components of the immune system. Nanoparticles can be engineered to either avoid immune system recognition or specifically inhibit or enhance the immune responses. We review herein reported observations on nanoparticle-mediated immunostimulation and immunosuppression, focusing on possible theories regarding how manipulation of particle physicochemical properties ...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3101232</comments>
            <pubDate>Wed, 16 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3101232</guid>        </item>
        <item>
            <title>Minireview: Nanoparticles for Molecular Imaging--An Overview.</title>
            <link>http://www.medworm.com/index.php?rid=3101231&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20016027%26dopt%3DAbstract</link>
            <description>Authors: Minchin RF, Martin DJ
    Molecular imaging is a technique for quantifying physiological changes in vivo using imaging probes, or beacons, which can be detected noninvasively. This field of study has advanced rapidly in recent years, in part due to the application of nanotechnology. The versatility of different imaging modalities has been significantly enhanced by innovative nanoparticle development. These nanoprobes can be used to image specific cells and tissues within a whole organism. Some of the nanoparticles under development may be useful to measure biological processes associated with human disease and help monitor how these change with treatment. This review highlights some of the recent advances in nanoparticles for molecular imaging. It also addresses issues that arise ...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3101231</comments>
            <pubDate>Wed, 16 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3101231</guid>        </item>
        <item>
            <title>Minireview: A Tiny Touch: Activation of Cell Signaling Pathways with Magnetic Nanoparticles.</title>
            <link>http://www.medworm.com/index.php?rid=3101230&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20016028%26dopt%3DAbstract</link>
            <description>Authors: Sniadecki NJ
    Magnetic nanoparticles can be coated with specific ligands that enable them to bind to receptors on a cell's surface. When a magnetic field is applied, it pulls on the particles so that they deliver nanoscale forces at the ligand-receptor bond. It has been observed that mechanical stimulation in this manner can activate cellular signaling pathways that are known as mechanotransduction pathways. Integrin receptors, stretch-activated ion channels, focal adhesions, and the cytoskeleton are key players in activating these pathways, but there is still much we do not know about how these mechanosensors work. Current evidence indicates that applied forces at these structures can activate Ca(2+) signaling, Src family protein kinase, MAPK, and RhoGTPase pathways. The techn...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3101230</comments>
            <pubDate>Wed, 16 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3101230</guid>        </item>
        <item>
            <title>7{alpha}-Hydroxytestosterone Affects 11{beta}-Hydroxysteroid Dehydrogenase 1 Direction in Rat Leydig Cells.</title>
            <link>http://www.medworm.com/index.php?rid=3101229&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20016029%26dopt%3DAbstract</link>
            <description>Authors: Hu GX, Lian QQ, Chen BB, Prasad PV, Kumar N, Zheng ZQ, Ge RS
    The cytochrome P450 2A1 (CYP2A1) is a P450 enzyme that catalyzes the metabolism of testosterone. CYP2A1 has been reported to be present in rat testis. However, its developmental changes and function have not been well characterized. The purpose of this study was to measure the abundance of CYP2A1 (Cyp2a1) mRNA in the developing rat testis and Leydig cells and examine the effects of its product, 7alpha-hydroxytestosterone (7HT), on an important enzyme, 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) that interconverts active corticosterone and inactive 11-dehydrocorticosterone. As detected by real-time PCR, Cyp2a1 was found to be present exclusively in the Leydig cell. CYP2A1 activity in adult Leydig cells wa...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3101229</comments>
            <pubDate>Wed, 16 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3101229</guid>        </item>
        <item>
            <title>Nutritional Programming Affects Hypothalamic Organization and Early Response to Leptin.</title>
            <link>http://www.medworm.com/index.php?rid=3101228&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20016030%26dopt%3DAbstract</link>
            <description>This study reveals the importance of an early catch-up growth that reduces abnormal organization of hypothalamic pathways involved in energy homeostasis, whereas protein restriction, maintained during postnatal development leads to an important immaturity of the hypothalamus.
    PMID: 20016030 [PubMed - as supplied by publisher] (Source: Endocrinology)</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3101228</comments>
            <pubDate>Wed, 16 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3101228</guid>        </item>
        <item>
            <title>Up-Regulating the Heme Oxygenase System with Hemin Improves Insulin Sensitivity and Glucose Metabolism in Adult Spontaneously Hypertensive Rats.</title>
            <link>http://www.medworm.com/index.php?rid=3101227&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20016031%26dopt%3DAbstract</link>
            <description>Authors: Ndisang JF, Lane N, Syed N, Jadhav A
    Accumulating clinical evidence indicates that impaired glucose tolerance is a common phenomenon in essential hypertension. Although recent evidence underscores the role of heme-oxygenase (HO) in diabetes, its effects on insulin sensitivity and glucose metabolism in spontaneously hypertensive rat (SHR), a model of essential hypertension with characteristics of metabolic syndrome including insulin resistance/impaired glucose metabolism remains largely unclear. Here we report the effects of the HO inducer, hemin, and the HO blocker, chromium-mesoporphyrin on insulin sensitivity and glucose metabolism in SHRs. Adult SHRs were severely hypertensive but normoglycemic. Hemin therapy lowered blood pressure, increased plasma insulin, decreased glyce...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3101227</comments>
            <pubDate>Wed, 16 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3101227</guid>        </item>
        <item>
            <title>Use of Mutant Mouse Lines to Investigate Origin of Gonadotropin-Releasing Hormone-1 Neurons: Lineage Independent of the Adenohypophysis.</title>
            <link>http://www.medworm.com/index.php?rid=3101235&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20008041%26dopt%3DAbstract</link>
            <description>In this report, single- and double-mutant mice were used to examine the lineage of GnRH-1 cells. GnRH is essential for vertebrate reproduction, with either GnRH-1 or GnRH-3 controlling release of gonadotropins from the anterior pituitary, depending on the species. It is clear that the neuroendocrine GnRH cells migrate from extracentral nervous system locations into the forebrain. However, the embryonic origin of GnRH-1 and GnRH-3 cells is controversial and has been suggested to be nasal placode, adenohypophyseal (anterior pituitary) placode, or neural crest, again dependent on the species examined. We found that mutant mice with either missing or disrupted anterior pituitaries (Gli2(-/-), Gli1(-/-)Gli2(-/-), and Lhx3(-/-)) exhibit a normal GnRH-1 neuronal population and that these cells ar...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3101235</comments>
            <pubDate>Fri, 11 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3101235</guid>        </item>
        <item>
            <title>Oxytocin Increases Glucose Uptake in Neonatal Rat Cardiomyocytes.</title>
            <link>http://www.medworm.com/index.php?rid=3101234&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20008042%26dopt%3DAbstract</link>
            <description>Authors: Florian M, Jankowski M, Gutkowska J
    We have recently shown that an entire oxytocin (OT) system, a peptide and its cognate receptors, is synthesized in the heart. In fetal and newborn hearts, OT exists in its extended three-amino acid form, OT-Gly-Lys-Arg (OT-GKR). OT translocates glucose transporter type 4 to the plasma membrane in human endothelial cells. Therefore, we hypothesized that the cardiac OT/OT-GKR system may be involved in the regulation of myocardial glucose uptake in physiological conditions and during metabolic stress such as hypoxia. Primary cultures of neonatal rat cardiomyocytes (CM) and cardiac progenitor cells expressing ATP-binding cassette efflux transporter G2 transporter (stem cell marker) were studied. OT (10 nM) increased basal glucose uptake in CM to...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3101234</comments>
            <pubDate>Fri, 11 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3101234</guid>        </item>
        <item>
            <title>Consequences of Monocarboxylate Transporter 8 Deficiency for Renal Transport and Metabolism of Thyroid Hormones in Mice.</title>
            <link>http://www.medworm.com/index.php?rid=3076322&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19996182%26dopt%3DAbstract</link>
            <description>Authors: Trajkovic-Arsic M, Visser TJ, Darras VM, Friesema EC, Schlott B, Mittag J, Bauer K, Heuer H
    Patients carrying inactivating mutations in the gene encoding the thyroid hormone transporting monocarboxylate transporter (MCT)-8 suffer from a severe form of psychomotor retardation and exhibit abnormal serum thyroid hormone levels. The thyroidal phenotype characterized by high-serum T3 and low-serum T4 levels is also found in mice mutants deficient in MCT8 although the cause of these abnormalities is still unknown. Here we describe the consequences of MCT8 deficiency for renal thyroid hormone transport, metabolism, and function by studying MCT8 null mice and wild-type littermates. Whereas serum and urinary parameters do not indicate a strongly altered renal function, a pronounced ind...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3076322</comments>
            <pubDate>Tue, 08 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3076322</guid>        </item>
        <item>
            <title>Hypothalamic Actions of Tumor Necrosis Factor {alpha} Provide the Thermogenic Core for the Wastage Syndrome in Cachexia.</title>
            <link>http://www.medworm.com/index.php?rid=3076321&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19996183%26dopt%3DAbstract</link>
            <description>Authors: Arruda AP, Milanski M, Romanatto T, Solon C, Coope A, Alberici LC, Festuccia WT, Hirabara SM, Ropelle E, Curi R, Carvalheira JB, Vercesi AE, Velloso LA
    TNFalpha is an important mediator of catabolism in cachexia. Most of its effects have been characterized in peripheral tissues, such as skeletal muscle and fat. However, by acting directly in the hypothalamus, TNFalpha can activate thermogenesis and modulate food intake. Here we show that high concentration TNFalpha in the hypothalamus leads to increased O2 consumption/CO2 production, increased body temperature, and reduced caloric intake, resulting in loss of body mass. Most of the thermogenic response is produced by beta3-adrenergic signaling to the brown adipose tissue (BAT), leading to increased BAT relative mass, reduction...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3076321</comments>
            <pubDate>Tue, 08 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3076321</guid>        </item>
        <item>
            <title>Epithelial Cell Transforming Protein 2 (ECT2) Depletion Blocks Polar Body Extrusion and Generates Mouse Oocytes Containing Two Metaphase II Spindles.</title>
            <link>http://www.medworm.com/index.php?rid=3076320&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19996184%26dopt%3DAbstract</link>
            <description>In conclusion, our study demonstrates the indispensable role of the maturation-promoting factor/ECT2/RhoA pathway in PBI extrusion in mouse oocytes.
    PMID: 19996184 [PubMed - as supplied by publisher] (Source: Endocrinology)</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3076320</comments>
            <pubDate>Tue, 08 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3076320</guid>        </item>
        <item>
            <title>Epigenetic Regulation of Estrogen Receptor {alpha} Gene Expression in the Mouse Cortex during Early Postnatal Development.</title>
            <link>http://www.medworm.com/index.php?rid=3076334&amp;cid=s_37679_15_f&amp;fid=37679&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19966177%26dopt%3DAbstract</link>
            <description>Authors: Westberry JM, Trout AL, Wilson ME
    Estrogens play a critical role in brain development by acting on areas that express estrogen receptors. In the rodent cortex, estrogen receptor alpha (ERalpha) mRNA expression is high early in postnatal development but declines starting at postnatal day (PND) 10 and is virtually absent in the adult cortex. The mechanisms controlling this regulation are largely unknown. Methylation is important for gene silencing during development in many tissues, including the brain. In the present study, we examined the methylation status of ERalpha 5' untranslated exons during early postnatal development in male and female mice using methylation-specific PCR and pyrosequencing. Several regions of ERalpha promoter displayed a significant increase in methylat...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3076334</comments>
            <pubDate>Fri, 04 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3076334</guid>        </item>
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