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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>Wed, 08 Feb 2012 15:08:56 +0100</lastBuildDate>
        <item>
            <title>Maternal consumption of high-fat diet disturbs hypothalamic neuronal function in the offspring: implications for the genesis of obesity.</title>
            <link>http://www.medworm.com/index.php?rid=5625959&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%3D22267682%26dopt%3DAbstract</link>
            <description>Authors: Velloso LA
    PMID: 22267682 [PubMed - in process] (Source: Endocrinology)</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5625959</comments>
            <pubDate>Wed, 25 Jan 2012 12:02:59 +0100</pubDate>
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        <item>
            <title>The Suprachiasmatic Nucleus Gets Split: Why Does Cortisol Respond But Not ACTH?</title>
            <link>http://www.medworm.com/index.php?rid=5625958&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%3D22267683%26dopt%3DAbstract</link>
            <description>Authors: Engeland WC, Yoder JM
    PMID: 22267683 [PubMed - in process] (Source: Endocrinology)</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5625958</comments>
            <pubDate>Wed, 25 Jan 2012 12:02:05 +0100</pubDate>
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        <item>
            <title>The foxo family: partners in crime or silent heroes.</title>
            <link>http://www.medworm.com/index.php?rid=5625957&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%3D22267684%26dopt%3DAbstract</link>
            <description>Authors: Estall JL
    PMID: 22267684 [PubMed - in process] (Source: Endocrinology)</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5625957</comments>
            <pubDate>Wed, 25 Jan 2012 12:01:39 +0100</pubDate>
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        <item>
            <title>A &quot;growing&quot; realization.</title>
            <link>http://www.medworm.com/index.php?rid=5625956&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%3D22267685%26dopt%3DAbstract</link>
            <description>A &quot;growing&quot; realization.
    Endocrinology. 2012 Feb;153(2):552-3
    Authors: Suter KJ
    PMID: 22267685 [PubMed - in process] (Source: Endocrinology)</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5625956</comments>
            <pubDate>Wed, 25 Jan 2012 12:01:06 +0100</pubDate>
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        <item>
            <title>Erratum.</title>
            <link>http://www.medworm.com/index.php?rid=5625955&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%3D22267686%26dopt%3DAbstract</link>
            <description>Authors: 
    PMID: 22267686 [PubMed - in process] (Source: Endocrinology)</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5625955</comments>
            <pubDate>Wed, 25 Jan 2012 12:00:35 +0100</pubDate>
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        <item>
            <title>Antiapolipoprotein A-1 IgG Chronotropic Effects Require Nongenomic Action of Aldosterone on L-Type Calcium Channels.</title>
            <link>http://www.medworm.com/index.php?rid=5605853&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%3D22253414%26dopt%3DAbstract</link>
            <description>In conclusion, our results indicate that, on NRVC, the aldosterone-dependent chronotropic effects of antiapoA-1 IgG involve the nongenomic activation of L-type calcium channels.
    PMID: 22253414 [PubMed - as supplied by publisher] (Source: Endocrinology)</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5605853</comments>
            <pubDate>Tue, 17 Jan 2012 05:00:00 +0100</pubDate>
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        <item>
            <title>Brown Fat Lipoatrophy and Increased Visceral Adiposity through a Concerted Adipocytokines Overexpression Induces Vascular Insulin Resistance and Dysfunction.</title>
            <link>http://www.medworm.com/index.php?rid=5605852&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%3D22253415%26dopt%3DAbstract</link>
            <description>In this study, we analyzed the role played by concerted expression of adipocytokines associated with brown fat lipoatrophy and increased visceral adiposity on triggering vascular insulin resistance and dysfunction in brown adipose tissue (BAT) insulin receptor knockout (BATIRKO) mice. In addition, we assessed whether vascular insulin resistance may aggravate vascular damage. The 52-wk-old, but not 33-wk-old, BATIRKO mice had a significant decrease of BAT mass associated with a significant increase of visceral white adipose tissue (WAT) mass, without changes in body weight. Brown fat lipoatrophy and increased visceral adiposity enhanced the concerted expression of adipocytokines (TNF-α, leptin, and plasminogen activator inhibitor 1) and nuclear factor-κB binding activity in BAT and viscer...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5605852</comments>
            <pubDate>Tue, 17 Jan 2012 05:00:00 +0100</pubDate>
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        <item>
            <title>Uncovering Novel Reproductive Defects in Neurokinin B Receptor Null Mice: Closing the Gap Between Mice and Men.</title>
            <link>http://www.medworm.com/index.php?rid=5605851&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%3D22253416%26dopt%3DAbstract</link>
            <description>Authors: Yang JJ, Caligioni CS, Chan YM, Seminara SB
    Abstract
    Patients bearing mutations in TAC3 and TACR3 (which encode neurokinin B and its receptor, respectively) have sexual infantilism and infertility due to GnRH deficiency. In contrast, Tacr3(-/-) mice have previously been reported to be fertile. Because of this apparent phenotypic discordance between mice and men bearing disabling mutations in Tacr3/TACR3, Tacr3 null mice were phenotyped with close attention to pubertal development, estrous cyclicity, and fertility. Tacr3(-/-) mice demonstrated normal timing of preputial separation and day of first estrus, markers of sexual maturation. However, at postnatal d 60, Tacr3(-/-) males had significantly smaller testes and lower FSH levels than their wild-type littermates. Tacr3(-/...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5605851</comments>
            <pubDate>Tue, 17 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5605851</guid>        </item>
        <item>
            <title>Angiotensin II-Dependent Transcriptional Activation of Human Steroidogenic Acute Regulatory Protein Gene by a 25-kDa cAMP-Responsive Element Modulator Protein Isoform and Yin Yang 1.</title>
            <link>http://www.medworm.com/index.php?rid=5605850&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%3D22253417%26dopt%3DAbstract</link>
            <description>Authors: Meier RK, Clark BJ
    Abstract
    Transcriptional activation of the steroidogenic acute regulatory protein (STAR) gene is a critical component in the angiotensin II (Ang II)-dependent increase in aldosterone biosynthesis in the adrenal gland. The purpose of this study was to define the molecular mechanisms that mediate the Ang II-dependent increase in STARD1 gene (STAR) expression in H295R human adrenocortical cells. Mutational analysis of the STAR proximal promoter revealed that a nonconsensus cAMP-responsive element located at -78 bp relative to the transcription start site (-78CRE) is required for the Ang II-stimulated STAR reporter gene activity. DNA immunoaffinity chromatography identified a 25-kDa cAMP-responsive element modulator isoform and Yin Yang 1 (YY1) as -78CRE DNA...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5605850</comments>
            <pubDate>Tue, 17 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5605850</guid>        </item>
        <item>
            <title>Activation of Southern White Rhinoceros (Ceratotherium simum simum) Estrogen Receptors by Phytoestrogens: Potential Role in the Reproductive Failure of Captive-Born Females?</title>
            <link>http://www.medworm.com/index.php?rid=5605849&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%3D22253418%26dopt%3DAbstract</link>
            <description>Authors: Tubbs C, Hartig P, Cardon M, Varga N, Milnes M
    Abstract
    The captive southern white rhinoceros (SWR; Ceratotherium simum simum) population serves as an important genetic reservoir critical to the conservation of this vulnerable species. Unfortunately, captive populations are declining due to the poor reproductive success of captive-born females. Captive female SWR exhibit reproductive problems suggested to result from continual ovarian follicular activity and prolonged exposure to endogenous estrogen. However, we investigated the potential role of exogenous dietary phytoestrogens in the reproductive failure of SWR by cloning and characterizing in vitro phytoestrogen binding and activation of recombinant SWR estrogen receptors (ESR). We compared those characteristics with re...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5605849</comments>
            <pubDate>Tue, 17 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5605849</guid>        </item>
        <item>
            <title>Peroxisome Proliferator-Activated Receptors-α and -γ, and cAMP-Mediated Pathways, Control Retinol-Binding Protein-4 Gene Expression in Brown Adipose Tissue.</title>
            <link>http://www.medworm.com/index.php?rid=5605848&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%3D22253419%26dopt%3DAbstract</link>
            <description>Authors: Rosell M, Hondares E, Iwamoto S, Gonzalez FJ, Wabitsch M, Staels B, Olmos Y, Monsalve M, Giralt M, Iglesias R, Villarroya F
    Abstract
    Retinol binding protein-4 (RBP4) is a serum protein involved in the transport of vitamin A. It is known to be produced by the liver and white adipose tissue. RBP4 release by white fat has been proposed to induce insulin resistance. We analyzed the regulation and production of RBP4 in brown adipose tissue. RBP4 gene expression is induced in brown fat from mice exposed to cold or treated with peroxisome proliferator-activated receptor (PPAR) agonists. In brown adipocytes in culture, norepinephrine, cAMP, and activators of PPARγ and PPARα induced RBP4 gene expression and RBP4 protein release. The induction of RBP4 gene expression by norepineph...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5605848</comments>
            <pubDate>Tue, 17 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5605848</guid>        </item>
        <item>
            <title>Early Postnatal Hyperalimentation Impairs Renal Function via SOCS-3 Mediated Renal Postreceptor Leptin Resistance.</title>
            <link>http://www.medworm.com/index.php?rid=5605847&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%3D22253420%26dopt%3DAbstract</link>
            <description>Authors: Alejandre Alcazar Miguel A, Boehler E, Rother E, Amann K, Vohlen C, von Hörsten S, Plank C, Dötsch J
    Abstract
    Early postnatal hyperalimentation has long-term implications for obesity and developing renal disease. Suppressor of cytokine signaling (SOCS) 3 inhibits phosphorylation of signal transducer and activator of transcription (STAT) 3 and ERK1/2 and thereby plays a pivotal role in mediating leptin resistance. In addition, SOCS-3 is induced by both leptin and inflammatory cytokines. However, little is known about the intrinsic-renal leptin synthesis and function. Therefore, this study aimed to elucidate the implications of early postnatal hyperalimentation on renal function and on the intrinsic-renal leptin signaling. Early postnatal hyperalimentation in Wistar rats d...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5605847</comments>
            <pubDate>Tue, 17 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5605847</guid>        </item>
        <item>
            <title>Phylogenetic Comparisons Implicate Sex Hormone-Binding Globulin in &quot;Masculinization&quot; of the Female Spotted Hyena (Crocuta crocuta).</title>
            <link>http://www.medworm.com/index.php?rid=5605846&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%3D22253421%26dopt%3DAbstract</link>
            <description>Phylogenetic Comparisons Implicate Sex Hormone-Binding Globulin in &quot;Masculinization&quot; of the Female Spotted Hyena (Crocuta crocuta).
    Endocrinology. 2012 Jan 17;
    Authors: Hammond GL, Miguel-Queralt S, Yalcinkaya TM, Underhill C, Place NJ, Glickman SE, Drea CM, Wagner AP, Siiteri PK
    Abstract
    Exposures to sex steroids during fetal development are thought to contribute to the unique urogenital anatomy and social dominance of the female spotted hyena: overt phenotypes not shared by other hyenids (i.e. striped hyena, brown hyena, and aardwolf). Because both androgens and estrogens influence development of genitalia and behavior, and because plasma SHBG regulates their access to tissues, we compared the Shbg gene sequences, structures, and steroid-binding properties in the four ext...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5605846</comments>
            <pubDate>Tue, 17 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5605846</guid>        </item>
        <item>
            <title>Molecular Characterization and Biological Function of Neuroendocrine Regulatory Peptide-3 in the Rat.</title>
            <link>http://www.medworm.com/index.php?rid=5605845&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%3D22253422%26dopt%3DAbstract</link>
            <description>Authors: Fujihara H, Sasaki K, Mishiro-Sato E, Ohbuchi T, Dayanithi G, Yamasaki M, Ueta Y, Minamino N
    Abstract
    Neuroendocrine regulatory peptide (NERP)-3, derived from the neurosecretory protein VGF (non-aconymic), is a new biologically active peptide identified through peptidomic analysis of the peptides secreted by an endocrine cell line. Using a specific antibody recognizing the C-terminal region of NERP-3, immunoreactive (ir)-NERP-3 was identified in acid extracts of rat brain and gut as a 30-residue NERP-3 with N-terminal pyroglutamylation. Assessed by radioimmunoassay, ir-NERP-3 was more abundant in the brain, including the posterior pituitary (PP), than in the gut. Immunohistochemistry demonstrated that ir-NERP-3 was significantly increased in the suprachiasmatic nucleus, th...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5605845</comments>
            <pubDate>Tue, 17 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5605845</guid>        </item>
        <item>
            <title>Improved Insulin Sensitivity after Long-Term Treatment with AT1 Blockers Is Not Associated with PPARγ Target Gene Regulation.</title>
            <link>http://www.medworm.com/index.php?rid=5605844&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%3D22253423%26dopt%3DAbstract</link>
            <description>Authors: Müller-Fielitz H, Landolt J, Heidbreder M, Werth S, Vogt FM, Jöhren O, Raasch W
    Abstract
    In both cell culture experiments and in vivo studies, a number of angiotensin II type 1 (AT(1)) receptor antagonists activated the peroxisome proliferator-activated receptor-γ (PPARγ). This mechanism has been discussed to be, at least in part, responsible for the improvement in glucose metabolism observed in animal studies and clinical trials. To investigate whether the PPARγ-dependent mechanism may represent a valid target for chronic therapy, spontaneously hypertensive rats (SHR) were fed either with a cafeteria diet (CD) or standard chow. CD-fed SHR were simultaneously treated with either telmisartan (TEL; 8 mg/kg(body weight)·d) or candesartan (CAND; 10 mg/kg(body weight)·d)...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5605844</comments>
            <pubDate>Tue, 17 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5605844</guid>        </item>
        <item>
            <title>Disruption of the Murine Glp2r Impairs Paneth Cell Function and Increases Susceptibility to Small Bowel Enteritis.</title>
            <link>http://www.medworm.com/index.php?rid=5605843&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%3D22253424%26dopt%3DAbstract</link>
            <description>Authors: Lee SJ, Lee J, Li KK, Holland D, Maughan H, Guttman DS, Yusta B, Drucker DJ
    Abstract
    Exogenous glucagon-like peptide-2 receptor (GLP-2R) activation elicits proliferative and cytoprotective responses in the gastrointestinal mucosa and ameliorates experimental small and large bowel gut injury. Nevertheless, the essential physiological role(s) of the endogenous GLP-2R remain poorly understood. We studied the importance of the GLP-2R for gut growth, epithelial cell lineage allocation, the response to mucosal injury, and host-bacterial interactions in Glp2r(-/-) and littermate control Glp2r(+/+) mice. Glp2r(-/-) mice exhibit normal somatic growth and preserved small and large bowel responses to IGF-I and keratinocyte growth factor. However, Glp2r(-/-) mice failed to up-regulate...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5605843</comments>
            <pubDate>Tue, 17 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5605843</guid>        </item>
        <item>
            <title>Antiapoptotic Actions of Exendin-4 against Hypoxia and Cytokines Are Augmented by CREB.</title>
            <link>http://www.medworm.com/index.php?rid=5605842&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%3D22253425%26dopt%3DAbstract</link>
            <description>The objective of the present study was to determine whether the cytoprotective actions of exendin-4 in human islets can be augmented by increasing the levels of CREB. Simulation of ischemia/reperfusion injury and exposure to hypoxic conditions in cultured human islets resulted in decreased CREB activation and induction of apoptosis. Islets were transduced with adenoviral CREB followed by exposure to exendin-4 as a strategy for improving their survival. This combination increased the levels of several proteins needed for β-cell survival and function, including insulin receptor substrate-2, Bcl-2, and baculoviral IAP repeat-containing 3, and suppressed the expression of proapoptotic and inflammatory genes. A combination of CREB and exendin-4 exerted enhanced antiapoptotic action in cultured...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5605842</comments>
            <pubDate>Tue, 17 Jan 2012 05:00:00 +0100</pubDate>
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        <item>
            <title>Expression and Regulation of Human Fetal-Specific CYP3A7 in Mice.</title>
            <link>http://www.medworm.com/index.php?rid=5605841&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%3D22253426%26dopt%3DAbstract</link>
            <description>Authors: Pang XY, Cheng J, Kim JH, Matsubara T, Krausz KW, Gonzalez FJ
    Abstract
    CYP3A7 is the predominant cytochrome P450 (CYP) expressed in human fetal liver, accounting for 30-50% of the total CYP in fetal liver and 87-100% of total fetal hepatic CYP3A content. However, the lack of a rodent model limits the investigation of CYP3A7 regulation and function. Hence, double-transgenic mice expressing human pregnane X receptor (PXR) and CYP3A4/7 (Tg3A4/7-hPXR) were used to investigate the regulation and function of CYP3A7. Expression of CYP3A7 was monitored in mice that ranged in age from 14.5-d-old embryos to 8.5-d-old newborns; expression of CYP3A7 mRNA was increased before birth in the embryos and decreased after birth in the newborns. This is consistent with the observed developmen...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5605841</comments>
            <pubDate>Tue, 17 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5605841</guid>        </item>
        <item>
            <title>Minireview: Epigenetics of Obesity and Diabetes in Humans.</title>
            <link>http://www.medworm.com/index.php?rid=5605840&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%3D22253427%26dopt%3DAbstract</link>
            <description>Authors: Slomko H, Heo HJ, Einstein FH
    Abstract
    Understanding the determinants of human health and disease is overwhelmingly complex, particularly for common, late-onset, chronic disorders, such as obesity and diabetes. Elucidating the genetic and environmental factors that influence susceptibility to disruptions in energy homeostasis and metabolic regulation remain a challenge, and progress will entail the integration of multiple assessments of temporally dynamic environmental exposures in the context of each individual's genotype. To meet this challenge, researchers are increasingly exploring the epigenome, which is the malleable interface of gene-environment interactions. Epigenetic variation, whether innate or induced, contributes to variation in gene expression, the range of p...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5605840</comments>
            <pubDate>Tue, 17 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5605840</guid>        </item>
        <item>
            <title>Physiological Responses to Acute Psychological Stress Are Reduced by the PPARγ Agonist Rosiglitazone.</title>
            <link>http://www.medworm.com/index.php?rid=5605839&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%3D22253428%26dopt%3DAbstract</link>
            <description>Authors: Ryan KK, Grayson BE, Jones KR, Schneider AL, Woods SC, Seeley RJ, Herman JP, Ulrich-Lai YM
    Abstract
    Physiological reactions to psychological stress are positively associated with several important chronic conditions including cardiovascular and neurodegenerative diseases and are linked to increased mortality. As such, the identification of cellular and molecular pathways that act to reduce stress responding may represent important targets for therapeutic intervention. Here we report that acute treatment with the peroxisome-proliferator activated receptor-γ (PPARγ) agonist rosiglitazone (RSG) blunts systemic responses to acute psychological stress in rats. Rats that had previously received oral RSG for 5 d exhibited a 40% reduction in the initial heart rate response to an...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5605839</comments>
            <pubDate>Tue, 17 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5605839</guid>        </item>
        <item>
            <title>Reduced Hippocampal Brain-Derived Neurotrophic Factor (BDNF) in Neonatal Rats after Prenatal Exposure to Propylthiouracil (PTU).</title>
            <link>http://www.medworm.com/index.php?rid=5605838&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%3D22253429%26dopt%3DAbstract</link>
            <description>Authors: Chakraborty G, Magagna-Poveda A, Parratt C, Umans JG, Maclusky NJ, Scharfman HE
    Abstract
    Thyroid hormone is critical for central nervous system development. Fetal hypothyroidism leads to reduced cognitive performance in offspring as well as other effects on neural development in both humans and experimental animals. The nature of these impairments suggests that thyroid hormone may exert its effects via dysregulation of the neurotrophin brain-derived neurotrophic factor (BDNF), which is critical to normal development of the central nervous system and has been implicated in neurodevelopmental disorders. The only evidence of BDNF dysregulation in early development, however, comes from experimental models in which severe prenatal hypothyroidism occurred. By contrast, milder pr...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5605838</comments>
            <pubDate>Tue, 17 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5605838</guid>        </item>
        <item>
            <title>Quantitative Measurement of Full-Length and C-Terminal Proteolyzed RBP4 in Serum of Normal and Insulin-Resistant Humans using a Novel Mass Spectrometry Immunoassay.</title>
            <link>http://www.medworm.com/index.php?rid=5605837&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%3D22253430%26dopt%3DAbstract</link>
            <description>Authors: Yang Q, Eskurza I, Kiernan UA, Phillips DA, Blüher M, Graham TE, Kahn BB
    Abstract
    Serum retinol-binding protein 4 (RBP4) levels are increased in insulin-resistant humans and correlate with severity of insulin resistance in metabolic syndrome. Quantitative Western blotting (qWestern) has been the most accurate method for serum RBP4 measurements, but qWestern is technically complex and labor intensive. The lack of a reliable, high-throughput method for RBP4 measurements has resulted in variability in findings in insulin-resistant humans. Many commonly used ELISAs have limited dynamic range. Neither the current ELISAs nor qWestern distinguish among full-length and carboxyl terminus proteolyzed forms of circulating RBP4 that are altered in different medical conditions. Here, ...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5605837</comments>
            <pubDate>Tue, 17 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5605837</guid>        </item>
        <item>
            <title>Thyroid Hormone Receptors Control Developmental Maturation of the Middle Ear and the Size of the Ossicular Bones.</title>
            <link>http://www.medworm.com/index.php?rid=5605836&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%3D22253431%26dopt%3DAbstract</link>
            <description>Authors: Cordas EA, Ng L, Hernandez A, Kaneshige M, Cheng SY, Forrest D
    Abstract
    Thyroid hormone is critical for auditory development and has well-known actions in the inner ear. However, less is known of thyroid hormone functions in the middle ear, which contains the ossicles (malleus, incus, stapes) that relay mechanical sound vibrations from the outer ear to the inner ear. During the later stages of middle ear development, prior to the onset of hearing, middle ear cavitation occurs, involving clearance of mesenchyme from the middle ear cavity while the immature cartilaginous ossicles attain appropriate size and ossify. Using in situ hybridization, we detected expression of Thra and Thrb genes encoding thyroid hormone receptors α1 and β (TRα1 and TRβ, respectively) in the imm...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5605836</comments>
            <pubDate>Tue, 17 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5605836</guid>        </item>
        <item>
            <title>Minireview: Epigenetic Programming of Diabetes and Obesity: Animal Models.</title>
            <link>http://www.medworm.com/index.php?rid=5605835&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%3D22253432%26dopt%3DAbstract</link>
            <description>Authors: Seki Y, Williams L, Vuguin PM, Charron MJ
    Abstract
    A growing body of evidence suggests that the intrauterine (IU) environment has a significant and lasting effect on the long-term health of the growing fetus and the development of metabolic disease in later life as put forth in the fetal origins of disease hypothesis. Metabolic diseases have been associated with alterations in the epigenome that occur without changes in the DNA sequence, such as cytosine methylation of DNA, histone posttranslational modifications, and micro-RNA. Animal models of epigenetic modifications secondary to an altered IU milieu are an invaluable tool to study the mechanisms that determine the development of metabolic diseases, such as diabetes and obesity. Rodent and nonlitter bearing animals are ...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5605835</comments>
            <pubDate>Tue, 17 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5605835</guid>        </item>
        <item>
            <title>Prediabetic Nephropathy as an Early Consequence of the High-Calorie/High-Fat Diet: Relation to Oxidative Stress.</title>
            <link>http://www.medworm.com/index.php?rid=5580025&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%3D22234462%26dopt%3DAbstract</link>
            <description>In conclusion, systemic and renal cortex oxidative stress associated with 12/15-lipoxygenase overexpression and activation is an early phenomenon caused by high-calorie/high-fat diet consumption and a likely contributor to kidney disease associated with prediabetes and alimentary obesity.
    PMID: 22234462 [PubMed - as supplied by publisher] (Source: Endocrinology)</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5580025</comments>
            <pubDate>Tue, 10 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5580025</guid>        </item>
        <item>
            <title>GLP-1 Receptor Agonists and the Thyroid: C-Cell Effects in Mice Are Mediated via the GLP-1 Receptor and not Associated with RET Activation.</title>
            <link>http://www.medworm.com/index.php?rid=5580024&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%3D22234463%26dopt%3DAbstract</link>
            <description>Authors: Madsen LW, Knauf JA, Gotfredsen C, Pilling A, Sjögren I, Andersen S, Andersen L, de Boer AS, Manova K, Barlas A, Vundavalli S, Berg Nyborg NC, Bjerre Knudsen L, Moelck AM, Fagin JA
    Abstract
    Liraglutide and exenatide are glucagon-like peptide receptor (GLP-1R) agonists used in the treatment of type 2 diabetes. Both molecules have been associated with the development of thyroid C-cell tumors after lifetime exposure in rodents. Previously, it has been reported that these tumors are preceded by increased plasma calcitonin and C-cell hyperplasia. We can now document that the murine C-cell effects are mediated via GLP-1R. Thus, 13 wk of continuous exposure to GLP-1R agonists was associated with marked increases in plasma calcitonin and in the incidence of C-cell hyperplasia in ...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5580024</comments>
            <pubDate>Tue, 10 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5580024</guid>        </item>
        <item>
            <title>Lipocalin 2 Deficiency Alters Estradiol Production and Estrogen Receptor Signaling in Female Mice.</title>
            <link>http://www.medworm.com/index.php?rid=5580023&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%3D22234464%26dopt%3DAbstract</link>
            <description>In this study, we reported the effect of Lcn2 deficiency on estradiol biosynthesis and estrogen receptor signaling in female Lcn2-deficient (Lcn2-/-) mice. We found that Lcn2 expression in white adipose tissue is gender, depot, and age dependent. In female mice, Lcn2 is predominantly expressed in inguinal adipose tissue but at relatively very low levels in perigonadal depot and ovary. After 22 wk of high-fat diet (HFD) feeding or at old age, Lcn2-/- female mice had significantly reduced levels of serum 17β-estradiol and down-regulated expression of estrogen receptor α in multiple metabolic tissues. Consistently, the expression of estrogen-regulated genes involved in cholesterol homeostasis, such as liver X receptor β and low-density lipoprotein receptor was also down-regulated in the ad...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5580023</comments>
            <pubDate>Tue, 10 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5580023</guid>        </item>
        <item>
            <title>Angiotensin II Reduces Food Intake by Altering Orexigenic Neuropeptide Expression in the Mouse Hypothalamus.</title>
            <link>http://www.medworm.com/index.php?rid=5580022&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%3D22234465%26dopt%3DAbstract</link>
            <description>Authors: Yoshida T, Semprun-Prieto L, Wainford RD, Sukhanov S, Kapusta DR, Delafontaine P
    Abstract
    Angiotensin II (Ang II), which is elevated in many chronic disease states such as end-stage renal disease and congestive heart failure, induces cachexia and skeletal muscle wasting by increasing muscle protein breakdown and reducing food intake. Neurohormonal mechanisms that mediate Ang II-induced appetite suppression are unknown. Consequently, we examined the effect of Ang II on expression of genes regulating appetite. Systemic Ang II (1 μg/kg · min) infusion in FVB mice rapidly reduced hypothalamic expression of neuropeptide Y (Npy) and orexin and decreased food intake at 6 h compared with sham-infused controls but did not change peripheral leptin, ghrelin, adiponectin, glucagon-l...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5580022</comments>
            <pubDate>Tue, 10 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5580022</guid>        </item>
        <item>
            <title>Conversion of TSH Heterodimer to a Single Polypeptide Chain Increases Bioactivity and Longevity.</title>
            <link>http://www.medworm.com/index.php?rid=5580021&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%3D22234466%26dopt%3DAbstract</link>
            <description>Authors: Azzam N, Bar-Shalom R, Fares F
    Abstract
    TSH is a dimeric glycoprotein hormone composed of a common α-subunit noncovalently linked to a hormone-specific β-subunit. Previously, the TSH heterodimer was successfully converted to an active single-chain hormone by genetically fusing α and β genes with [TSHβ- carboxyl-terminal peptide (CTP)-α] or without (TSHβ-α) the CTP of human chorionic gonadotropin β-subunit as a linker. In the present study, TSH variants were expressed in Chinese hamster ovarian cells. The results indicated that TSHβ-α single chain has the highest binding affinity to TSH receptor and the highest in vitro bioactivity. With regard to the in vivo bioactivity, all TSH variants increased the levels of T(4) in circulation after 2 and 4 h of treatment. H...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5580021</comments>
            <pubDate>Tue, 10 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5580021</guid>        </item>
        <item>
            <title>Differential Regulation of Glucose Transporters Mediated by CRH Receptor Type 1 and Type 2 in Human Placental Trophoblasts.</title>
            <link>http://www.medworm.com/index.php?rid=5580020&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%3D22234467%26dopt%3DAbstract</link>
            <description>Authors: Gao L, Lv C, Xu C, Li Y, Cui X, Gu H, Ni X
    Abstract
    Glucose transport across the placenta is mediated by glucose transporters (GLUT), which is critical for normal development and survival of the fetus. Regulatory mechanisms of GLUT in placenta have not been elucidated. Placental CRH has been implicated to play a key role in the control of fetal growth and development. We hypothesized that CRH, produced locally in placenta, could act to modulate GLUT in placenta. To investigate this, we obtained human placentas from uncomplicated term pregnancies and isolated and cultured trophoblast cells. GLUT1 and GLUT3 expressions in placenta were determined, and effects of CRH on GLUT1 and GLUT3 were examined. GLUT1 and GLUT3 were identified in placental villous syncytiotrophoblasts an...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5580020</comments>
            <pubDate>Tue, 10 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5580020</guid>        </item>
        <item>
            <title>Blockade of Cannabinoid Receptor 1 Improves Insulin Resistance, Lipid Metabolism, and Diabetic Nephropathy in db/db Mice.</title>
            <link>http://www.medworm.com/index.php?rid=5580019&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%3D22234468%26dopt%3DAbstract</link>
            <description>Authors: Nam DH, Lee MH, Kim JE, Song HK, Kang YS, Lee JE, Kim HW, Cha JJ, Hyun YY, Kim SH, Han SY, Han KH, Han JY, Cha DR
    Abstract
    The endocannabinoid system is important in the pathogenesis of obesity-related metabolic disorders. However, the effect of inhibiting the endocannabinoid system in type 2 diabetic nephropathy is unclear. Therefore, we examined the effect of the cannabinoid (CB)1 receptor antagonist, SR141716, on insulin resistance and diabetic nephropathy in db/db mice. Six-week-old db/db mice were treated with the CB1-specific antagonist SR141716 (10 mg/kg·d) for 3 months. Treatment with SR141716 significantly improved insulin resistance and lipid abnormalities. Concomitantly, CB1 antagonism improved cardiac functional and morphological abnormality, hepatic steatosis...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5580019</comments>
            <pubDate>Tue, 10 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5580019</guid>        </item>
        <item>
            <title>Activation of Latent Human GDF9 by a Single Residue Change (Gly391Arg) in the Mature Domain.</title>
            <link>http://www.medworm.com/index.php?rid=5580018&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%3D22234469%26dopt%3DAbstract</link>
            <description>In this study, we show that prodomain interactions differentially regulate the activity of GDF9 across species, such that murine (m) GDF9 is secreted in an active form, whereas human (h) GDF9 is latent. To understand this distinction, we used site-directed mutagenesis to introduce nonconserved mGDF9 residues into the pro- and mature domains of hGDF9. Activity-based screens of the resultant mutants indicated that a single mature domain residue (Gly(391)) confers latency to hGDF9. Gly(391) forms part of the type I receptor binding site on hGDF9, and this residue is present in all species except mouse, rat, hamster, galago, and possum, in which it is substituted with an arginine. In an adrenocortical cell luciferase assay, hGDF9 (Gly(391)Arg) had similar activity to mGDF9 (EC(50) 55 ng/ml vs....</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5580018</comments>
            <pubDate>Tue, 10 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5580018</guid>        </item>
        <item>
            <title>Mineralocorticoid Receptor Overexpression Facilitates Differentiation and Promotes Survival of Embryonic Stem Cell-Derived Neurons.</title>
            <link>http://www.medworm.com/index.php?rid=5580017&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%3D22234470%26dopt%3DAbstract</link>
            <description>Authors: Munier M, Law F, Meduri G, Le Menuet D, Lombès M
    Abstract
    Mineralocorticoid receptor (MR), highly expressed in the hippocampus, binds corticosteroid hormones and coordinately participates, with the glucocorticoid receptor, to the control of stress responses, memorization, and behavior. To investigate the impact of MR in neuronal survival, we generated murine embryonic stem (ES) cells that overexpress human MR (hMR) (P1-hMR) and are induced to differentiate into mature neurons. We showed that recombinant MR expression increased throughout differentiation and is 2-fold higher in P1-hMR ES-derived neurons compared with wild-type controls, whereas glucocorticoid receptor expression was unaffected. Although proliferation and early neuronal differentiation were comparable in P1...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5580017</comments>
            <pubDate>Tue, 10 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5580017</guid>        </item>
        <item>
            <title>Glucocorticoid Receptor Signaling Is Essential for Mesoderm Formation and Muscle Development in Zebrafish.</title>
            <link>http://www.medworm.com/index.php?rid=5580016&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%3D22234471%26dopt%3DAbstract</link>
            <description>Authors: Nesan D, Kamkar M, Burrows J, Scott IC, Marsden M, Vijayan MM
    Abstract
    Glucocorticoid receptor (GR) signaling is thought to play a key role in embryogenesis, but its specific developmental effects remain unclear. Cortisol is the primary ligand for GR activation in teleosts, and in zebrafish (Danio rerio), the prehatch embryo content of this steroid is of maternal origin. Using early zebrafish developmental stages, we tested the hypothesis that GR signaling is critical for embryo growth and hatching. In zebrafish, maternal GR mRNA is degraded quickly, followed by zygotic synthesis of the receptor. GR protein is widely expressed throughout early development, and we were able to knockdown this protein using morpholino oligonucleotides. This led to a more than 70% reduction in...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5580016</comments>
            <pubDate>Tue, 10 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5580016</guid>        </item>
        <item>
            <title>Norepinephrine, Active Norepinephrine Transporter, and Norepinephrine-Metabolism Are Involved in the Generation of Reactive Oxygen Species in Human Ovarian Granulosa Cells.</title>
            <link>http://www.medworm.com/index.php?rid=5580015&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%3D22234472%26dopt%3DAbstract</link>
            <description>Authors: Saller S, Merz-Lange J, Raffael S, Hecht S, Pavlik R, Thaler C, Berg D, Berg U, Kunz L, Mayerhofer A
    Abstract
    The neurotransmitter norepinephrine (NE) is derived from the sympathetic nervous system and may be involved in the regulation of ovarian functions. Ovarian innervation increases in patients with polycystic ovarian syndrome (PCOS), prompting us to readdress a role of NE in the human ovary. In vitro fertilization-derived granulosa cells (GC), follicular fluids (FF), and ovarian sections were studied. NE was found in FF and freshly isolated GC, yet significantly lower levels of NE were detected in samples from PCOS patients. Furthermore, the metabolite normetanephrine was detected in FF. Together this suggests cellular uptake and metabolism of NE in GC. In accordance,...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5580015</comments>
            <pubDate>Tue, 10 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5580015</guid>        </item>
        <item>
            <title>Minireview: NAD+, a circadian metabolite with an epigenetic twist.</title>
            <link>http://www.medworm.com/index.php?rid=5537718&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%3D22186411%26dopt%3DAbstract</link>
            <description>Authors: Sassone-Corsi P
    Abstract
    A wide variety of endocrine, physiological, and metabolic functions follow daily oscillations. Most of these regulations are controlled at the level of gene expression by the circadian clock and, a remarkably coordinated transcription-translation machinery that exerts its function in virtually all mammalian cells. A large fraction of the genome is under control of the circadian clock, a regulation that is achieved through dynamic changes in chromatin states. Recent findings have demonstrated intimate connections between the circadian clock and epigenetic control. The case of nicotinamide adenine dinucleotide, which modulates the circadian activity of the deacetylase sirtuin 1, constitutes a paradigmatic example of the link between cyclic cellular m...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5537718</comments>
            <pubDate>Sun, 25 Dec 2011 02:49:36 +0100</pubDate>
            <guid isPermaLink="false">5537718</guid>        </item>
        <item>
            <title>A novel antiinflammatory role for the short-chain Fatty acids in human labor.</title>
            <link>http://www.medworm.com/index.php?rid=5537712&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%3D22186417%26dopt%3DAbstract</link>
            <description>This study investigated the expression of G protein-coupled receptors GPR43 and GPR41 receptors in human uteroplacental tissues and the role of short-chain fatty acids (SCFA) in modulating inflammatory pathways in fetal membranes. Expression of GPR43 and GPR41 was investigated in uteroplacental tissues collected from women delivering at term or preterm after ethical approval and patient informed consent. The effect of SCFA on expression of inflammatory genes was assessed in amnion explants after culture with a mimetic of infection (lipopolysaccharide, LPS). Sodium propionate effect on LPS-induced neutrophil chemotaxis was evaluated by transwell assay. GPR43 and GPR41 mRNA expression was higher in myometrium and fetal membranes collected from women after the onset of labor. GPR43 protein ex...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5537712</comments>
            <pubDate>Sun, 25 Dec 2011 02:48:34 +0100</pubDate>
            <guid isPermaLink="false">5537712</guid>        </item>
        <item>
            <title>Erratum.</title>
            <link>http://www.medworm.com/index.php?rid=5537710&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%3D22194423%26dopt%3DAbstract</link>
            <description>Authors: 
    PMID: 22194423 [PubMed - in process] (Source: Endocrinology)</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5537710</comments>
            <pubDate>Sun, 25 Dec 2011 02:48:13 +0100</pubDate>
            <guid isPermaLink="false">5537710</guid>        </item>
        <item>
            <title>Overexpression of FoxO1 in the Hypothalamus and Pancreas Causes Obesity and Glucose Intolerance.</title>
            <link>http://www.medworm.com/index.php?rid=5537722&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%3D22186407%26dopt%3DAbstract</link>
            <description>Authors: Kim HJ, Kobayashi M, Sasaki T, Kikuchi O, Amano K, Kitazumi T, Lee YS, Yokota-Hashimoto H, Susanti VY, Kitamura YI, Nakae J, Kitamura T
    Abstract
    Recent studies have revealed that insulin signaling in pancreatic β-cells and the hypothalamus is critical for maintaining nutrient and energy homeostasis, the failure of which are hallmarks of metabolic syndrome. We previously reported that forkhead transcription factor forkhead box-containing protein of the O subfamily (FoxO)1, a downstream effector of insulin signaling, plays important roles in β-cells and the hypothalamus when we investigated the roles of FoxO1 independently in the pancreas and hypothalamus. However, because metabolic syndrome is caused by the combined disorders in hypothalamus and pancreas, to elucidate the...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5537722</comments>
            <pubDate>Tue, 20 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5537722</guid>        </item>
        <item>
            <title>Curcumin Down-Regulates Visfatin Expression and Inhibits Breast Cancer Cell Invasion.</title>
            <link>http://www.medworm.com/index.php?rid=5537721&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%3D22186408%26dopt%3DAbstract</link>
            <description>Authors: Kim SR, Park HJ, Bae YH, Ahn SC, Wee HJ, Yun I, Jang HO, Bae MK, Bae SK
    Abstract
    Obesity is frequently associated with breast cancer. Such associations are possibly mediated by adipokines. Visfatin, an adipokine, has recently been shown to be related to the development and progression of breast cancer. Therefore, the down-regulation of visfatin may be a novel strategy for breast cancer therapy. Curcumin has anticancer activities by modulating multiple signaling pathways and genes. The purpose of this study was to investigate whether visfatin gene expression is affected by curcumin in human breast cancer cells and to characterize the functional role of visfatin in breast cancer. We found that the mRNA and protein levels of visfatin were down-regulated by curcumin in MDA-MB-...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5537721</comments>
            <pubDate>Tue, 20 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5537721</guid>        </item>
        <item>
            <title>Cbx2, a Polycomb Group Gene, Is Required for Sry Gene Expression in Mice.</title>
            <link>http://www.medworm.com/index.php?rid=5537720&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%3D22186409%26dopt%3DAbstract</link>
            <description>Authors: Katoh-Fukui Y, Miyabayashi K, Komatsu T, Owaki A, Baba T, Shima Y, Kidokoro T, Kanai Y, Schedl A, Wilhelm D, Koopman P, Okuno Y, Morohashi KI
    Abstract
    Mice lacking the function of the polycomb group protein CBX2 (chromobox homolog 2; also known as M33) show defects in gonadal, adrenal, and splenic development. In particular, XY knockout (KO) mice develop ovaries but not testes, and the gonads are hypoplastic in both sexes. However, how CBX2 regulates development of these tissues remains largely unknown. In the present study, we used microarray, RT-PCR, and immunohistochemical analyses to show that the expression of Sry, Sox9, Lhx9, Ad4BP/SF-1, Dax-1, Gata4, Arx, and Dmrt1, genes encoding transcription factors essential for gonadal development, is affected in Cbx2 KO gonads...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5537720</comments>
            <pubDate>Tue, 20 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5537720</guid>        </item>
        <item>
            <title>Disruption of the Chemokine-Like Receptor-1 (CMKLR1) Gene Is Associated with Reduced Adiposity and Glucose Intolerance.</title>
            <link>http://www.medworm.com/index.php?rid=5537719&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%3D22186410%26dopt%3DAbstract</link>
            <description>Authors: Ernst MC, Haidl ID, Zúñiga LA, Dranse HJ, Rourke JL, Zabel BA, Butcher EC, Sinal CJ
    Abstract
    Adipose tissue secretes a variety of bioactive signaling molecules, termed adipokines, which regulate numerous biological functions including appetite, energy balance, glucose homeostasis, and inflammation. Chemerin is a novel adipokine that regulates adipocyte differentiation and metabolism by binding to and activating the G protein-coupled receptor, chemokine like receptor-1 (CMKLR1). In the present study, we investigated the impact of CMKLR1 deficiency on adipose development, glucose homeostasis, and inflammation in vivo. Herein we report that regardless of diet (low or high fat), CMKLR1(-/-) mice had lower food consumption, total body mass, and percent body fat compared with ...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5537719</comments>
            <pubDate>Tue, 20 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5537719</guid>        </item>
        <item>
            <title>ERK Signaling, But Not c-Raf, Is Required for Gonadotropin-Releasing Hormone (GnRH)-Induced Regulation of Nur77 in Pituitary Gonadotropes.</title>
            <link>http://www.medworm.com/index.php?rid=5537717&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%3D22186412%26dopt%3DAbstract</link>
            <description>Authors: Bliss SP, Navratil AM, Xie J, Miller A, Baccarini M, Roberson MS
    Abstract
    Stimulation of pituitary gonadotropes by hypothalamic GnRH leads to the rapid expression of several immediate early genes that play key roles in orchestrating the response of the gonadotrope to hypothalamic stimuli. Elucidation of the signaling mechanisms that couple the GnRH receptor to this immediate early gene repertoire is critical for understanding the molecular basis of GnRH action. Here we identify signaling mechanisms that underlie regulation of the orphan nuclear receptor Nur77 as a GnRH-responsive immediate early gene in αT3-1 cells and mouse gonadotropes in culture. Using a variety of approaches, we show that GnRH-induced transcriptional upregulation of Nur77 in αT3-1 cells is dependent ...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5537717</comments>
            <pubDate>Tue, 20 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5537717</guid>        </item>
        <item>
            <title>Novel Biological Action of the Dipeptidylpeptidase-IV Inhibitor, Sitagliptin, as a Glucagon-Like Peptide-1 Secretagogue.</title>
            <link>http://www.medworm.com/index.php?rid=5537716&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%3D22186413%26dopt%3DAbstract</link>
            <description>Authors: Sangle GV, Lauffer LM, Grieco A, Trivedi S, Iakoubov R, Brubaker PL
    Abstract
    Glucagon-like peptide-1 (GLP-1) is an incretin hormone secreted into the circulation by the intestinal L cell. The dipeptidylpeptidase-IV (DPP-IV) inhibitor, sitagliptin, prevents GLP-1 degradation and is used in the clinic to treat patients with type 2 diabetes mellitus, leading to improved glycated hemoglobin levels. When the effect of sitagliptin on GLP-1 levels was examined in neonatal streptozotocin rats, a model of type 2 diabetes mellitus, a 4.9 ± 0.9-fold increase in basal and 3.6 ± 0.4-fold increase in oral glucose-stimulated plasma levels of active GLP-1 was observed (P &amp;lt; 0.001), in association with a 1.5 ± 0.1-fold increase in the total number of intestinal L cells (P &amp;lt; 0.01). ...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5537716</comments>
            <pubDate>Tue, 20 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5537716</guid>        </item>
        <item>
            <title>Galectin-9 and T Cell Immunoglobulin Mucin-3 Pathway Is a Therapeutic Target for Type 1 Diabetes.</title>
            <link>http://www.medworm.com/index.php?rid=5537715&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%3D22186414%26dopt%3DAbstract</link>
            <description>Authors: Kanzaki M, Wada J, Sugiyama K, Nakatsuka A, Teshigawara S, Murakami K, Inoue K, Terami T, Katayama A, Eguchi J, Akiba H, Yagita H, Makino H
    Abstract
    Galectin-9 (Gal-9), a ligand for T cell Ig mucin-3 (Tim-3), induces apoptosis in cluster of differentiation 4 (CD4)(+) Tim-3(+) T helper 1 (T(H)1) cells via the Gal-9-Tim-3 pathway and negatively regulates T(H)1 immunity. In turn, Gal-9 activates dendritic cells (DC) to produce TNF-α, which promotes the T(H)1 response. We investigated the efficacy of Gal-9 against T(H)1-mediated autoimmune diabetes in NOD mice and compared with anti-Tim-3 monoclonal antibody (RMT3-23), which inhibited the binding between Tim-3-Ig and Gal-9 in a solid-phase binding assay. mRNA expression of Gal-9 was prominently induced by the treatment of int...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5537715</comments>
            <pubDate>Tue, 20 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5537715</guid>        </item>
        <item>
            <title>Adrenal Cell Aldosterone Production Is Stimulated by Very-Low-Density Lipoprotein (VLDL).</title>
            <link>http://www.medworm.com/index.php?rid=5537714&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%3D22186415%26dopt%3DAbstract</link>
            <description>In conclusion, we have shown that VLDL can stimulate aldosterone synthesis in adrenocortical cells by increasing StAR and CYP11B2 expression, an event likely mediated by a calcium-initiated signaling cascade.
    PMID: 22186415 [PubMed - as supplied by publisher] (Source: Endocrinology)</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5537714</comments>
            <pubDate>Tue, 20 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5537714</guid>        </item>
        <item>
            <title>Corncob Bedding Alters the Effects of Estrogens on Aggressive Behavior and Reduces Estrogen Receptor-α Expression in the Brain.</title>
            <link>http://www.medworm.com/index.php?rid=5537713&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%3D22186416%26dopt%3DAbstract</link>
            <description>Authors: Villalon Landeros R, Morisseau C, Yoo HJ, Fu SH, Hammock BD, Trainor BC
    Abstract
    There is growing appreciation that estrogen signaling pathways can be modulated by naturally occurring environmental compounds such as phytoestrogens and the more recently discovered xenoestrogens. Many researchers studying the effects of estrogens on brain function or behavior in animal models choose to use phytoestrogen-free food for this reason. Corncob bedding is commonly used in animal facilities across the United States and has been shown to inhibit estrogen-dependent reproductive behavior in rats. The mechanism for this effect was unclear, because the components of corncob bedding mediating this effect did not bind estrogen receptors. Here, we show in the California mouse (Peromyscus ca...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5537713</comments>
            <pubDate>Tue, 20 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5537713</guid>        </item>
        <item>
            <title>Anxiolytic Effects and Neuroanatomical Targets of Estrogen Receptor-β (ERβ) Activation by a Selective ERβ Agonist in Female Mice.</title>
            <link>http://www.medworm.com/index.php?rid=5537711&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%3D22186418%26dopt%3DAbstract</link>
            <description>We examined the effects of the biologically active S-enantiomer of diarylpropionitrile (S-DPN) on anxiety-related behavioral measures, the corresponding stress hormonal response to hypothalamo-pituitary-adrenal axis reactivity, and potential sites of neuronal activation in mutant female mice carrying a null mutation for ERβ gene (βERKO). S-DPN administration significantly reduced anxiety-like behaviors in the open field, light-dark exploration, and the elevated plus maze (EPM) in ovariectomized wild-type (WT) mice, but not in their βERKO littermates. Stress-induced corticosterone (CORT) and ACTH were also attenuated by S-DPN in the WT mice but not in the βERKO mice. Using c-fos induction after elevated plus maze, as a marker of stress-induced neuronal activation, we identified the ante...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5537711</comments>
            <pubDate>Tue, 20 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5537711</guid>        </item>
        <item>
            <title>Allopregnanolone Prevents Dieldrin-Induced NMDA Receptor Internalization and Neurotoxicity by Preserving GABAA Receptor Function.</title>
            <link>http://www.medworm.com/index.php?rid=5515379&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%3D22166974%26dopt%3DAbstract</link>
            <description>Authors: Briz V, Parkash J, Sánchez-Redondo S, Prevot V, Suñol C
    Abstract
    Dieldrin is an endocrine disruptor that accumulates in mammalian adipose tissue and brain. It induces convulsions due to its antagonism of the γ-aminobutyric acid A receptor (GABA(A)R). We have previously reported that long-term exposure to dieldrin causes the internalization of the N-methyl-d-aspartate receptor (NMDAR) as a result of persistent GABA(A)R inhibition. Because the neurosteroids 17β-estradiol (E2) and allopregnanolone are known to modulate the function and trafficking of GABA(A)R and NMDAR, we examined the effects of E2 and allopregnanolone on dieldrin-induced GABA(A)R inhibition, NMDAR internalization, and neuronal death in cortical neurons. We found that 1 nm E2 increased the membrane expre...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5515379</comments>
            <pubDate>Tue, 13 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5515379</guid>        </item>
        <item>
            <title>Glucose-Mediated Repression of Menin Promotes Pancreatic β-Cell Proliferation.</title>
            <link>http://www.medworm.com/index.php?rid=5515378&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%3D22166975%26dopt%3DAbstract</link>
            <description>In this study, we found that the menin level was significantly reduced in high glucose-treated INS1 cells and primary rat islets, both with increased proliferation. A similar observation was found in islets isolated from rats subjected to 72-h continuous glucose infusion. The glucose-induced proliferation was inhibited by menin overexpression. Further molecular studies showed that glucose-induced menin suppression was blocked by PI3K/Akt pathway inhibitors. A major PI3K/Akt substrate, Foxo1, was shown to enhance menin transcription levels by binding the promoter region of the Men1 gene. Therefore, we conclude that glucose inhibits menin expression via the PI3K/Akt/Foxo1 pathway and hence promotes pancreatic β-cell proliferation. Our study suggests that menin might serve as an important in...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5515378</comments>
            <pubDate>Tue, 13 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5515378</guid>        </item>
        <item>
            <title>Rapid Estrogen Receptor-Mediated Mechanisms Determine the Sexually Dimorphic Sensitivity of Ventricular Myocytes to 17β-Estradiol and the Environmental Endocrine Disruptor Bisphenol A.</title>
            <link>http://www.medworm.com/index.php?rid=5515377&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%3D22166976%26dopt%3DAbstract</link>
            <description>Authors: Belcher SM, Chen Y, Yan S, Wang HS
    Abstract
    Previously we showed that 17β-estradiol (E(2)) and/or the xenoestrogen bisphenol A (BPA) alter ventricular myocyte Ca(2+) handing, resulting in increased cardiac arrhythmias in a female-specific manner. In the present study, the roles of estrogen receptors (ER) in mediating the rapid contractile and arrhythmogenic effects of estrogens were examined. Contractility was used as an index to assess the impact of E(2) or BPA on Ca(2+) handling in rodent ventricular myocytes. The concentration-response curve for the stimulatory effects of BPA and E(2) on female myocyte was inverted-U shaped. Detectable effects for each compound were observed at 10(-12) m, and the most efficacious concentrations for each were at 10(-9) m. Sensitivity to...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5515377</comments>
            <pubDate>Tue, 13 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5515377</guid>        </item>
        <item>
            <title>Growth Hormone Stimulates Transcription of the Fibroblast Growth Factor 21 Gene in the Liver through the Signal Transducer and Activator of Transcription 5.</title>
            <link>http://www.medworm.com/index.php?rid=5515376&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%3D22166977%26dopt%3DAbstract</link>
            <description>In this study, we tested the hypothesis that FGF21 gene expression in the liver is controlled by GH through STAT5. We found that GH injection to cattle increased FGF21 mRNA expression in the liver. Mapped by a 5'-rapid amplification of cDNA ends assay, transcription of the FGF21 gene in the bovine liver was mainly initiated from a nucleotide 24 bp downstream of a TATA box. The bovine FGF21 promoter contains three putative STAT5-binding sites. EMSA confirmed the ability of them to bind to liver STAT5 protein from GH-injected cattle. Chromatin immunoprecipitation assays demonstrated that GH administration increased the binding of STAT5 to the FGF21 promoter in the liver. Cotransfection analyses showed that GH induced reporter gene expression from the FGF21 promoter in a STAT5-dependent manne...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5515376</comments>
            <pubDate>Tue, 13 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5515376</guid>        </item>
        <item>
            <title>Developmental Changes in GnRH Release in Response to Kisspeptin Agonist and Antagonist in Female Rhesus Monkeys (Macaca mulatta): Implication for the Mechanism of Puberty.</title>
            <link>http://www.medworm.com/index.php?rid=5515375&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%3D22166978%26dopt%3DAbstract</link>
            <description>In this study, we examined the effects of the KP agonist, human KP-10 (hKP-10), and the KP antagonist, peptide 234, on in vivo GnRH release in prepubertal and pubertal ovarian-intact female rhesus monkeys using a microdialysis method. We found that direct infusion of hKP-10 into the medial basal hypothalamus and stalk-median eminence region stimulated GnRH release in a dose-responsive manner, whereas infusion of peptide 234 suppressed GnRH release in both developmental stages. Because ovarian steroid feedback on GnRH release becomes prominent after the initiation of puberty in primates, we further examined whether ovarian steroids modify the GnRH response to hKP-10. Results demonstrate that the hKP-10-induced stimulation of GnRH release was eliminated by ovariectomy in pubertal, but not pr...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5515375</comments>
            <pubDate>Tue, 13 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5515375</guid>        </item>
        <item>
            <title>The Clock Gene Rev-erbα Regulates Pancreatic β-Cell Function: Modulation by Leptin and High-Fat Diet.</title>
            <link>http://www.medworm.com/index.php?rid=5515374&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%3D22166979%26dopt%3DAbstract</link>
            <description>Authors: Vieira E, Marroquí L, Batista TM, Caballero-Garrido E, Carneiro EM, Boschero AC, Nadal A, Quesada I
    Abstract
    Disturbances of circadian rhythms have been associated with obesity and type 2 diabetes. The nuclear receptor Rev-erbα was suggested to link circadian rhythms and metabolism in peripheral tissues. The aim of the present study was to dissect the role of this clock gene in the pancreatic β-cell function and to analyze whether its expression is modulated by leptin and diet-induced obesity. To address the function of Rev-erbα, we used small interfering RNA in mouse islet cells and in MIN-6 cells. Cell proliferation was measured by bromodeoxyuridine incorporation, apoptosis by the terminal deoxynucleotidyl transferase dUTP nick end labeling technique, insulin secreti...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5515374</comments>
            <pubDate>Tue, 13 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5515374</guid>        </item>
        <item>
            <title>Twist Modulates Human Trophoblastic Cell Invasion via Regulation of N-Cadherin.</title>
            <link>http://www.medworm.com/index.php?rid=5515373&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%3D22166980%26dopt%3DAbstract</link>
            <description>Authors: Ng YH, Zhu H, Leung PC
    Abstract
    The invasion of extravillous cytotrophoblasts (EVT) into the underlying maternal tissues and vasculature is a key step in human placentation. The molecular mechanisms involved in the development of the invasive phenotype of EVT include many that were first discovered for their role in cancer cell metastasis. Previous studies have demonstrated that N-cadherin and its regulatory transcription factor Twist play important roles in the onset and progression of cancers, but their roles in human trophoblastic cell invasion is not clear. The goal of the study was to examine the role of Twist and N-cadherin in human trophoblastic cell invasion. Twist and N-cadherin mRNA and protein levels were determined by RT-PCR and Western blotting in human placen...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5515373</comments>
            <pubDate>Tue, 13 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5515373</guid>        </item>
        <item>
            <title>Social Status Predicts How Sex Steroid Receptors Regulate Complex Behavior across Levels of Biological Organization.</title>
            <link>http://www.medworm.com/index.php?rid=5515372&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%3D22166981%26dopt%3DAbstract</link>
            <description>Authors: O'Connell LA, Hofmann HA
    Abstract
    Social status strongly affects behavior and physiology, in part mediated by gonadal hormones, although how each sex steroid acts across levels of biological organization is not well understood. We examine the role of sex steroids in modulating social behavior in dominant (DOM) and subordinate (SUB) males of a highly social fish, Astatotilapia burtoni. We first used agonists and antagonists to each sex steroid receptor and found that androgens and progestins modulate courtship behavior only in DOM, whereas estrogens modulate aggressive behavior independent of social status. We then examined the hormonal and physiological responses to sex steroid receptor antagonist treatment and uncovered substantial changes in circulating steroid hormone l...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5515372</comments>
            <pubDate>Tue, 13 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5515372</guid>        </item>
        <item>
            <title>Contribution of Nutritional Deficit to the Pathogenesis of the Nonthyroidal Illness Syndrome in Critical Illness: A Rabbit Model Study.</title>
            <link>http://www.medworm.com/index.php?rid=5515371&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%3D22166982%26dopt%3DAbstract</link>
            <description>In conclusion, in this rabbit model of sustained critical illness, reduced circulating T(3), but not T(4), levels could be prevented by parenteral nutrition, which may be mediated by leptin and its actions on tissue deiodinase activity.
    PMID: 22166982 [PubMed - as supplied by publisher] (Source: Endocrinology)</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5515371</comments>
            <pubDate>Tue, 13 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5515371</guid>        </item>
        <item>
            <title>B-Cell Maturation Antigen (BCMA) Activation Exerts Specific Proinflammatory Effects in Normal Human Keratinocytes and Is Preferentially Expressed in Inflammatory Skin Pathologies.</title>
            <link>http://www.medworm.com/index.php?rid=5515370&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%3D22166983%26dopt%3DAbstract</link>
            <description>Authors: Alexaki VI, Pelekanou V, Notas G, Venihaki M, Kampa M, Dessirier V, Sabour-Alaoui S, Stathopoulos EN, Tsapis A, Castanas E
    Abstract
    TNFα is known to be expressed in human skin, regulating immune-related responses. Here we report that human normal skin keratinocytes express the members of the TNF superfamily members A proliferation-inducing ligand (APRIL; TNFSF13), B cell-activating factor (BAFF; TNFSF13B), and their receptors, B cell maturation antigen (BCMA; TNFRSF17) and transmembrane activator, calcium-modulator, and cyclophilin ligand interactor (TACI; TNFRSF13B), in a distinct spatial pattern. Our data show a differential expression of these molecules within epidermal layers and skin appendages, whereas the BAFF-specific receptor BAFFR (TNFRSF13C) is absent. Importan...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5515370</comments>
            <pubDate>Tue, 13 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5515370</guid>        </item>
        <item>
            <title>Defining POMC Neurons Using Transgenic Reagents: Impact of Transient Pomc Expression in Diverse Immature Neuronal Populations.</title>
            <link>http://www.medworm.com/index.php?rid=5515369&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%3D22166984%26dopt%3DAbstract</link>
            <description>Authors: Padilla SL, Reef D, Zeltser LM
    Abstract
    Melanocortin signaling plays a central role in the regulation of phenotypes related to body weight and energy homeostasis. To specifically target and study the function of proopiomelanocortin (POMC) neurons, Pomc promoter elements have been utilized to generate reporter and Cre recombinase transgenic reagents. Across gestation, we find that Pomc is dynamically expressed in many sites in the developing mouse forebrain, midbrain, hindbrain, spinal cord, and retina. Although Pomc expression in most embryonic brain regions is transient, it is sufficient to direct Cre-mediated recombination of floxed alleles. We visualize the populations affected by this transgene by crossing Pomc-Cre mice to ROSA reporter strains and identify 62 sites of...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5515369</comments>
            <pubDate>Tue, 13 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5515369</guid>        </item>
        <item>
            <title>Glucagon in the Pathogenesis of Hypoglycemia and Hyperglycemia in Diabetes.</title>
            <link>http://www.medworm.com/index.php?rid=5515368&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%3D22166985%26dopt%3DAbstract</link>
            <description>Authors: Cryer PE
    Abstract
    Pancreatic islet α-cell glucagon secretion is critically dependent on pancreatic islet β-cell insulin secretion. Normally, a decrease in the plasma glucose concentration causes a decrease in β-cell insulin secretion that signals an increase in α-cell glucagon secretion during hypoglycemia. In contrast, an increase in the plasma glucose concentration, among other stimuli, causes an increase in β-cell insulin secretion that signals a decrease, or at least no change, in α-cell glucagon secretion after a meal. In absolute endogenous insulin deficiency (i.e. in type 1 diabetes and in advanced type 2 diabetes), however, β-cell failure results in no decrease in β-cell insulin secretion and thus no increase in α-cell glucagon secretion during hypoglycemi...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5515368</comments>
            <pubDate>Tue, 13 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5515368</guid>        </item>
        <item>
            <title>Hepatic Suppression of Foxo1 and Foxo3 Causes Hypoglycemia and Hyperlipidemia in Mice.</title>
            <link>http://www.medworm.com/index.php?rid=5515391&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%3D22147007%26dopt%3DAbstract</link>
            <description>In this study, we used the Cre/LoxP genetic approach to delete the Foxo1, Foxo3, and Foxo4 genes individually or a combination of two or all in the liver of lean or db/db mice and assessed the role of Foxo inactivation in regulating glucose and lipid homeostasis in vivo. In the lean mice or db/db mice, hepatic deletion of Foxo1, rather than Foxo3 or Foxo4, caused a modest reduction in blood glucose concentrations and barely affected lipid homeostasis. Combined deletion of Foxo1 and Foxo3 decreased blood glucose levels, elevated serum triglyceride and cholesterol concentrations, and increased hepatic lipid secretion and caused hepatosteatosis. Analysis of the liver transcripts established a prominent role of Foxo1 in regulating gene expression of gluconeogenic enzymes and Foxo3 in the expre...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5515391</comments>
            <pubDate>Tue, 06 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5515391</guid>        </item>
        <item>
            <title>Glucagon-Like Peptide-1 Enhances Glucokinase Activity in Pancreatic β-Cells through the Association of Epac2 with Rim2 and Rab3A.</title>
            <link>http://www.medworm.com/index.php?rid=5515390&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%3D22147008%26dopt%3DAbstract</link>
            <description>Authors: Park JH, Kim SJ, Park SH, Son DG, Bae JH, Kim HK, Han J, Song DK
    Abstract
    Glucokinase (GK), which phosphorylates d-glucose, is a major glucose sensor in β-cells for glucose-stimulated insulin secretion (GSIS) and is a promising new drug target for type 2 diabetes (T2D). In T2D, pancreatic β-cells exhibit defective glucose sensitivity, which leads to impaired GSIS. Although glucagon-like peptide-1-(7-36)-amide (GLP-1) is known to enhance β-cell glucose sensitivity, the effect of GLP-1 on GK activity is still unknown. The present study demonstrated that GLP-1 pretreatment for 30 min significantly enhanced GK activity in a glucose-dependent manner, with a lower Michaelis-Menten constant (K(m)) but unchanged maximal velocity (V(max)). Thus, GLP-1 acutely enhanced cellular g...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5515390</comments>
            <pubDate>Tue, 06 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5515390</guid>        </item>
        <item>
            <title>Liganded Thyroid Hormone Receptor Induces Nucleosome Removal and Histone Modifications to Activate Transcription during Larval Intestinal Cell Death and Adult Stem Cell Development.</title>
            <link>http://www.medworm.com/index.php?rid=5515389&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%3D22147009%26dopt%3DAbstract</link>
            <description>Authors: Matsuura K, Fujimoto K, Fu L, Shi YB
    Abstract
    Thyroid hormone (T(3)) plays an important role in regulating multiple cellular and metabolic processes, including cell proliferation, cell death, and energy metabolism, in vertebrates. Dysregulation of T(3) signaling results in developmental abnormalities, metabolic defects, and even cancer. We used T(3)-dependent Xenopus metamorphosis as a model to study how T(3) regulates transcription during vertebrate development. T(3) exerts its metamorphic effects through T(3) receptors (TR). TR recruits, in a T(3)-dependent manner, cofactor complexes that can carry out chromatin remodeling/histone modifications. Whether and how histone modifications change upon gene regulation by TR during vertebrate development is largely unknown. Here ...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5515389</comments>
            <pubDate>Tue, 06 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5515389</guid>        </item>
        <item>
            <title>Thyroid Hormone Receptor-α Gene Knockout Mice Are Protected from Diet-Induced Hepatic Insulin Resistance.</title>
            <link>http://www.medworm.com/index.php?rid=5515388&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%3D22147010%26dopt%3DAbstract</link>
            <description>In conclusion, loss of Thra protects mice from high-fat diet-induced hepatic steatosis and hepatic and peripheral insulin resistance. Therefore, thyroid receptor-α inhibition represents a novel pharmacologic target for the treatment of NAFLD, obesity, and type 2 diabetes.
    PMID: 22147010 [PubMed - as supplied by publisher] (Source: Endocrinology)</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5515388</comments>
            <pubDate>Tue, 06 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5515388</guid>        </item>
        <item>
            <title>Somatostatin Inhibition of GnRH Neuronal Activity and the Morphological Relationship between GnRH and Somatostatin Neurons in Rats.</title>
            <link>http://www.medworm.com/index.php?rid=5515387&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%3D22147011%26dopt%3DAbstract</link>
            <description>In this study, we assessed the morphological relationship between GnRH and somatostatin neurons. Confocal microscopy on the sections from the medial septum through medial preoptic area revealed about 35 close contacts per rat between the GnRH and somatostatin neuronal fibers in the organum vasculosum of the lamina terminalis region. No contact of somatostatin fibers on the GnRH neuronal somata was observed. Multicell RT-PCR for somatostatin receptor mRNA in rat GnRH neurons was also performed, which revealed moderate expression of somatostatin receptor subtypes 1-5. In addition, patch clamp experiments were carried out in acute slice preparations. Somatostatin suppressed neuronal firing in cells recorded in a cell-attached configuration and also induced whole-cell outward currents in GnRH ...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5515387</comments>
            <pubDate>Tue, 06 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5515387</guid>        </item>
        <item>
            <title>Differential Responses of Progesterone Receptor Membrane Component-1 (Pgrmc1) and the Classical Progesterone Receptor (Pgr) to 17β-Estradiol and Progesterone in Hippocampal Subregions that Support Synaptic Remodeling and Neurogenesis.</title>
            <link>http://www.medworm.com/index.php?rid=5515386&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%3D22147012%26dopt%3DAbstract</link>
            <description>We examined the neuronal expression of progesterone receptor membrane component-1 (Pgrmc1) and the classical progesterone receptor (Pgr), by in situ hybridization and immunohistochemistry. Pgr, a transcription factor, has been associated with synaptic remodeling and other major actions of P4, whereas Pgrmc1 is implicated in P4-dependent proliferation of adult neuroprogenitor cells and with rapid P4 effects on membranes. Ovariectomized adult rats were given E2, P4, or E2+P4 on two schedules: a 4-d model of the rodent estrous cycle and a 30-d model of postmenopausal hormone therapy. Pgr was hormonally responsive only in CA1 pyramidal neurons, and the induction of Pgr by E2 was partly antagonized by P4 only on the 30-d schedule. In CA3 pyramidal and dentate gyrus (DG) neurons, Pgr was largely...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5515386</comments>
            <pubDate>Tue, 06 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5515386</guid>        </item>
        <item>
            <title>Impact of Ovarian Sex Steroids on Ovulation and Ovulatory Gene Induction in Aromatase-Null Mice.</title>
            <link>http://www.medworm.com/index.php?rid=5515385&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%3D22147013%26dopt%3DAbstract</link>
            <description>Authors: Toda K, Hayashi Y, Ono M, Saibara T
    Abstract
    Female mice deficient in the aromatase gene [aromatase knockout (ArKO)] fail to ovulate owing to an inability to produce estrogens. Here, we demonstrated that sequential administration of adequate amounts of 17β-estradiol (E2), pregnant mare serum gonadotropin, and human chorionic gonadotropin could induce ovulation in immature ArKO mice; nevertheless, significantly fewer oocytes were released into the oviducts in ArKO mice than in wild-type mice. Analysis of ovarian steroids by liquid chromatography coupled with electrospray ionization-tandem mass spectrometry identified a trace amount of E2 in the untreated immature ArKO ovary. The analysis further detected significant increases and decreases in progesterone and testosterone ...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5515385</comments>
            <pubDate>Tue, 06 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5515385</guid>        </item>
        <item>
            <title>Zinc Depletion Causes Multiple Defects in Ovarian Function during the Periovulatory Period in Mice.</title>
            <link>http://www.medworm.com/index.php?rid=5515384&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%3D22147014%26dopt%3DAbstract</link>
            <description>Authors: Tian X, Diaz FJ
    Abstract
    Shortly before ovulation, the oocyte acquires developmental competence and granulosa cells undergo tremendous changes including cumulus expansion and luteinization. Zinc is emerging as a key regulator of meiosis in vitro, but a complete understanding of zinc-mediated effects during the periovulatory period is lacking. The present study uncovers the previously unknown role of zinc in maintaining meiotic arrest before ovulation. A zinc chelator [N,N,N',N'-tetrakis (2-pyridylmethyl) ethylenediamine (TPEN)] caused premature germinal vesicle breakdown and associated spindle defects in denuded oocytes even in the presence of a phosphodiesterase 3A inhibitor (milrinone). TPEN also potently blocked cumulus expansion by blocking induction of expansion-relat...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5515384</comments>
            <pubDate>Tue, 06 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5515384</guid>        </item>
        <item>
            <title>Hypothalamic JNK1 and IKKβ Activation and Impaired Early Postnatal Glucose Metabolism after Maternal Perinatal High-Fat Feeding.</title>
            <link>http://www.medworm.com/index.php?rid=5515383&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%3D22147015%26dopt%3DAbstract</link>
            <description>In this study, virgin female C57BL/6 mice received high-fat feeding starting at conception until weaning of the offspring at postnatal d 21. The offspring developed increased body weight, body fat content, and serum leptin concentrations during the nursing period. Analysis of hypothalamic tissue of the offspring at postnatal d 21 showed up-regulation of several members of the toll-like receptor 4 signaling cascade and subsequent activation of c-Jun N-terminal kinase 1 and IκB kinase-β inflammatory pathways. Interestingly, glucose tolerance testing in the offspring revealed signs of impaired glucose tolerance along with increased hepatic expression of the key gluconeogenic enzyme phosphoenolpyruvate carboxykinase. In addition, significantly increased hepatic and pancreatic PGC1α expressi...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5515383</comments>
            <pubDate>Tue, 06 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5515383</guid>        </item>
        <item>
            <title>Exposure to Di(2-ethyl-hexyl) phthalate (DEHP) in Utero and during Lactation Causes Long-Term Pituitary-Gonadal Axis Disruption in Male and Female Mouse Offspring.</title>
            <link>http://www.medworm.com/index.php?rid=5515382&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%3D22147016%26dopt%3DAbstract</link>
            <description>In conclusion, our findings suggest that, in maternally exposed male and female mice, DEHP acts on multiple pathways involved in maintaining steroid homeostasis. Specifically, in utero and lactational DEHP exposure may alter estrogen synthesis in both sexes. This, in turn, induces dysregulation of pituitary-gonadal feedback and alters the reproductive performance of exposed animals.
    PMID: 22147016 [PubMed - as supplied by publisher] (Source: Endocrinology)</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5515382</comments>
            <pubDate>Tue, 06 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5515382</guid>        </item>
        <item>
            <title>VEGFA Family Isoforms Regulate Spermatogonial Stem Cell Homeostasis in Vivo.</title>
            <link>http://www.medworm.com/index.php?rid=5515381&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%3D22147017%26dopt%3DAbstract</link>
            <description>The objective of the present study was to investigate vascular endothelial growth factor A (VEGFA) isoform regulation of cell fate decisions of spermatogonial stem cells (SSC) in vivo. The expression pattern and cell-specific distribution of VEGF isoforms, receptors, and coreceptors during testis development postnatal d 1-180 suggest a nonvascular function for VEGF regulation of early germ cell homeostasis. Populations of undifferentiated spermatogonia present shortly after birth were positive for VEGF receptor activation as demonstrated by immunohistochemical analysis. Thus, we hypothesized that proangiogenic isoforms of VEGF (VEGFA(164)) stimulate SSC self-renewal, whereas antiangiogenic isoforms of VEGF (VEGFA(165)b) induce differentiation of SSC. To test this hypothesis, we used transp...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5515381</comments>
            <pubDate>Tue, 06 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5515381</guid>        </item>
        <item>
            <title>Circadian Feeding Drive of Metabolic Activity in Adipose Tissue and not Hyperphagia Triggers Overweight in Mice: Is There a Role of the Pentose-Phosphate Pathway?</title>
            <link>http://www.medworm.com/index.php?rid=5515380&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%3D22147018%26dopt%3DAbstract</link>
            <description>Authors: Stucchi P, Gil-Ortega M, Merino B, Guzmán-Ruiz R, Cano V, Valladolid-Acebes I, Somoza B, Le Gonidec S, Argente J, Valet P, Chowen JA, Fernández-Alfonso M, Ruiz-Gayo M
    Abstract
    High-fat (HF) diets trigger an increase in adipose tissue and body weight (BW) and disordered eating behavior. Our study deals with the hypothesis that circadian distribution of energy intake is more relevant for BW dynamics than diet composition. Four-week-old mice were exposed for 8 wk to a HF diet and compared with animals receiving control chow. HF mice progressively increased BW, decreased the amount of nocturnal (1800-0900 h) calories (energy or food intake) (30%) and increased diurnal (0900-1800 h) caloric intake (energy or food intake), although total daily intake was identical between grou...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5515380</comments>
            <pubDate>Tue, 06 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5515380</guid>        </item>
        <item>
            <title>In memoriam: john d. Baxter, m.d., 1940-2011.</title>
            <link>http://www.medworm.com/index.php?rid=5515411&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%3D22116999%26dopt%3DAbstract</link>
            <description>Authors: 
    PMID: 22116999 [PubMed - in process] (Source: Endocrinology)</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5515411</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5515411</guid>        </item>
        <item>
            <title>How does an anabolic/androgenic steroid get banned from sport competition?</title>
            <link>http://www.medworm.com/index.php?rid=5515410&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%3D22117000%26dopt%3DAbstract</link>
            <description>Authors: Rogol AD
    PMID: 22117000 [PubMed - in process] (Source: Endocrinology)</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5515410</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5515410</guid>        </item>
        <item>
            <title>Polyuria, polydipsia, and poly(a) tails: insights into the adaptive nature of the cellular stress response pathways.</title>
            <link>http://www.medworm.com/index.php?rid=5515409&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%3D22117001%26dopt%3DAbstract</link>
            <description>Authors: Leng G, Skehel P
    PMID: 22117001 [PubMed - in process] (Source: Endocrinology)</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5515409</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5515409</guid>        </item>
        <item>
            <title>Hear, hear! Thyroid hormone transporters in cochlear development.</title>
            <link>http://www.medworm.com/index.php?rid=5515408&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%3D22117002%26dopt%3DAbstract</link>
            <description>Authors: Heuer H
    PMID: 22117002 [PubMed - in process] (Source: Endocrinology)</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5515408</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5515408</guid>        </item>
        <item>
            <title>Erratum.</title>
            <link>http://www.medworm.com/index.php?rid=5515407&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%3D22117003%26dopt%3DAbstract</link>
            <description>Authors: 
    PMID: 22117003 [PubMed - in process] (Source: Endocrinology)</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5515407</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5515407</guid>        </item>
        <item>
            <title>Deletion of Tuberous Sclerosis 1 in Somatic Cells of the Murine Reproductive Tract Causes Female Infertility.</title>
            <link>http://www.medworm.com/index.php?rid=5515406&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%3D22128018%26dopt%3DAbstract</link>
            <description>We examined whether conditional deletion of TSC1 by a knock-in allele of the anti-Müllerian hormone type 2 receptor (Amhr2) driving Cre expression and subsequent activation of mTOR in granulosa cells and in oviductal and uterine stromal cells affects fertility in female mice. Increased phosphorylation of ribosomal protein S6, a downstream target of activated mTOR, was observed in all AMHR2-expressing tissues examined, indicating loss of TSC1 activity. TSC1 deletion in granulosa cells led to the detection of significantly fewer primordial follicles in mutant mice at 12 wk, suggesting premature ovarian insufficiency, which might be related to the significantly increased time mutant mice spent in estrus. Although the number of good-quality ovulated oocytes was not significantly different com...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5515406</comments>
            <pubDate>Tue, 29 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5515406</guid>        </item>
        <item>
            <title>Intranasal Leptin Reduces Appetite and Induces Weight Loss in Rats with Diet-Induced Obesity (DIO).</title>
            <link>http://www.medworm.com/index.php?rid=5515405&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%3D22128019%26dopt%3DAbstract</link>
            <description>Authors: Schulz C, Paulus K, Jöhren O, Lehnert H
    Abstract
    Resistance to brain-mediated effects of leptin is a characteristic feature of obesity, resulting from alterations in leptin receptor signaling in hypothalamic neurons and/or transport across the blood-brain-barrier. We have shown previously, that the latter can be circumvented by intranasal (i.n.) application of leptin in lean rats. This prompted us to test i.n. leptin in animals with diet-induced obesity (DIO) as a basis for future human administration. DIO was induced in male Wistar rats by feeding a cafeteria diet for 25 or 32 wk, respectively. Consecutively, these DIO animals (seven to eight per treatment) and standard diet rats (lean) (14-15 per treatment, matched for age and diet duration) were treated with 0.1, 0.2 m...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5515405</comments>
            <pubDate>Tue, 29 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5515405</guid>        </item>
        <item>
            <title>Sex Differences in the Metabolic Effects of Testosterone in Sheep.</title>
            <link>http://www.medworm.com/index.php?rid=5515404&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%3D22128020%26dopt%3DAbstract</link>
            <description>Authors: Clarke SD, Clarke IJ, Rao A, Cowley MA, Henry BA
    Abstract
    Adiposity is regulated in a sexually divergent manner. This is partly due to sex steroids, but the differential effects of androgens in males and females are unclear. We investigated effects of testosterone on energy balance in castrated male (n = 6) and female sheep (n = 4), which received 3 × 200 mg testosterone implants for 2 wk or blank implants (controls). Temperature probes were implanted into retroperitoneal fat and skeletal muscle. Blood samples were taken to measure metabolites and insulin. In males, muscle and fat biopsies were collected to measure uncoupling protein (UCP) mRNA and phosphorylation of AMP-activated protein kinase and Akt. Testosterone did not change food intake in either sex. Temperature i...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5515404</comments>
            <pubDate>Tue, 29 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5515404</guid>        </item>
        <item>
            <title>A Single-Nucleotide Polymorphism in the EAP1 Gene Is Associated with Amenorrhea/Oligomenorrhea in Nonhuman Primates.</title>
            <link>http://www.medworm.com/index.php?rid=5515403&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%3D22128021%26dopt%3DAbstract</link>
            <description>Authors: Lomniczi A, Garcia-Rudaz C, Ramakrishnan R, Wilmot B, Khouangsathiene S, Ferguson B, Dissen GA, Ojeda SR
    Abstract
    Current evidence suggests that the acquisition of female reproductive capacity and the maintenance of mature reproductive function are related processes transcriptionally regulated by gene networks operating within the neuroendocrine brain. One of these genes, termed enhanced at puberty 1 (EAP1), encodes an upstream regulator of these processes. Selective inhibition of EAP1 expression in discrete regions of the rat and nonhuman primate (NHP) hypothalamus, via targeted delivery of RNA interference, either disrupts (rats) or abolishes (monkeys) reproductive cycles. The striking loss of menstrual cyclicity resulting from knocking down hypothalamic EAP1 expression ...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5515403</comments>
            <pubDate>Tue, 29 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5515403</guid>        </item>
        <item>
            <title>Hypothalamic EAP1 (Enhanced at Puberty 1) Is Required for Menstrual Cyclicity in Nonhuman Primates.</title>
            <link>http://www.medworm.com/index.php?rid=5515402&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%3D22128022%26dopt%3DAbstract</link>
            <description>Authors: Dissen GA, Lomniczi A, Heger S, Neff TL, Ojeda SR
    Abstract
    Mammalian reproductive cyclicity requires the periodic discharge of GnRH from hypothalamic neurons into the portal vessels connecting the neuroendocrine brain to the pituitary gland. GnRH secretion is, in turn, controlled by changes in neuronal and glial inputs to GnRH-producing neurons. The transcriptional control of this process is not well understood, but it appears to involve several genes. One of them, termed enhanced at puberty 1 (EAP1), has been postulated to function in the female hypothalamus as an upstream regulator of neuroendocrine reproductive function. RNA interference-mediated inhibition of EAP1 expression, targeted to the preoptic region, delays puberty and disrupts estrous cyclicity in rodents, sug...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5515402</comments>
            <pubDate>Tue, 29 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5515402</guid>        </item>
        <item>
            <title>Identification of an Enhancer in the Ad4BP/SF-1 Gene Specific for Fetal Leydig Cells.</title>
            <link>http://www.medworm.com/index.php?rid=5515401&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%3D22128023%26dopt%3DAbstract</link>
            <description>Authors: Shima Y, Miyabayashi K, Baba T, Otake H, Oka S, Zubair M, Morohashi KI
    Abstract
    Adrenal 4 binding protein/steroidogenic factor 1 (Ad4BP/SF-1) (Nr5a1) is a nuclear receptor essential for reproductive tissue development and endocrine regulation. This factor is expressed in steroidogenic tissues (e.g. adrenal glands and gonads), and expression of this factor is tightly regulated in a tissue and cell type-specific manner. Our previous studies have identified tissue and cell type-specific enhancers in the introns of the Ad4BP/SF-1 gene in fetal adrenal glands, ventromedial hypothalamus, and pituitary gonadotrope. Characterization of the enhancers had provided new insights into tissue and cell development. However, these studies have failed to identify any gonad-specific enhance...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5515401</comments>
            <pubDate>Tue, 29 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5515401</guid>        </item>
        <item>
            <title>Disassociation between Preprandial Gut Peptide Release and Food-Anticipatory Activity.</title>
            <link>http://www.medworm.com/index.php?rid=5515400&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%3D22128024%26dopt%3DAbstract</link>
            <description>Authors: Dailey MJ, Stingl KC, Moran TH
    Abstract
    Animals learn to anticipate a meal as evidenced by increases in premeal activity. This learned response appears to be independent of the nutrient status of an animal because food-anticipatory activity (FAA) can be seen after entrainment by a highly palatable food when rats remain ad libitum on chow. Mealtime feeding not only induces an increase in activity but also appears to entrain the secretion of various peptides prior to a meal including insulin, ghrelin, and glucagon-like peptide-1 (GLP-1). It is not clear whether these meal-anticipatory changes in peptides are causally associated with FAA. To assess whether FAA and preprandial peptide changes co-occur with meal entrainment using different diets, rats were conditioned to receiv...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5515400</comments>
            <pubDate>Tue, 29 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5515400</guid>        </item>
        <item>
            <title>Protection from Palmitate-Induced Mitochondrial DNA Damage Prevents from Mitochondrial Oxidative Stress, Mitochondrial Dysfunction, Apoptosis, and Impaired Insulin Signaling in Rat L6 Skeletal Muscle Cells.</title>
            <link>http://www.medworm.com/index.php?rid=5515399&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%3D22128025%26dopt%3DAbstract</link>
            <description>Authors: Yuzefovych LV, Solodushko VA, Wilson GL, Rachek LI
    Abstract
    Saturated free fatty acids have been implicated in the increase of oxidative stress, mitochondrial dysfunction, apoptosis, and insulin resistance seen in type 2 diabetes. The purpose of this study was to determine whether palmitate-induced mitochondrial DNA (mtDNA) damage contributed to increased oxidative stress, mitochondrial dysfunction, apoptosis, impaired insulin signaling, and reduced glucose uptake in skeletal muscle cells. Adenoviral vectors were used to deliver the DNA repair enzyme human 8-oxoguanine DNA glycosylase/(apurinic/apyrimidinic) lyase (hOGG1) to mitochondria in L6 myotubes. After palmitate exposure, we evaluated mtDNA damage, mitochondrial function, production of mitochondrial reactive oxygen ...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5515399</comments>
            <pubDate>Tue, 29 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5515399</guid>        </item>
        <item>
            <title>Amelioration of Diabetic Neuropathy by TAT-Mediated Enhanced Delivery of Metallothionein and SOD.</title>
            <link>http://www.medworm.com/index.php?rid=5515398&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%3D22128026%26dopt%3DAbstract</link>
            <description>Authors: Min D, Kim H, Park L, Kim TH, Hwang S, Kim MJ, Jang S, Park Y
    Abstract
    Because diabetic neuropathy (DN) appears to result from oxidative stress in neuronal tissues, antioxidant treatment should counteract the condition. Metallothionein (MT) and superoxide dismutase (SOD) are free-radical scavengers, but their ability to cross biological membranes is limited. Applying cell penetrating peptide technologies, we made Tat-MT and Tat-SOD constructs and tested their ability to protect PC12 cells, as surrogates of peripheral nerve cells, from various forms of oxidative damage. Tat-MT and Tat-SOD were successfully delivered to PC12 cells, and the intracellular activities of MT and SOD increased in line with the amount of protein delivered. These agents inhibited cellular damage and...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5515398</comments>
            <pubDate>Tue, 29 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5515398</guid>        </item>
        <item>
            <title>Acute Stress Increases the Synthesis of 7α-Hydroxypregnenolone, a New Key Neurosteroid Stimulating Locomotor Activity, through Corticosterone Action in Newts.</title>
            <link>http://www.medworm.com/index.php?rid=5515397&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%3D22128027%26dopt%3DAbstract</link>
            <description>Authors: Haraguchi S, Koyama T, Hasunuma I, Okuyama SI, Ubuka T, Kikuyama S, Do Rego JL, Vaudry H, Tsutsui K
    Abstract
    7α-Hydroxypregnenolone (7α-OH PREG) is a newly identified bioactive neurosteroid stimulating locomotor activity in the brain of newt, a wild animal, which serves as an excellent model to investigate the biosynthesis and biological action of neurosteroids. Here, we show that acute stress increases 7α-OH PREG synthesis in the dorsomedial hypothalamus (DMH) through corticosterone (CORT) action in newts. A 30-min restraint stress increased 7α-OH PREG synthesis in the brain tissue concomitant with the increase in plasma CORT concentrations. A 30-min restraint stress also increased the expression of cytochrome P450(7α) (CYP7B), the steroidogenic enzyme of 7α-OH PREG...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5515397</comments>
            <pubDate>Tue, 29 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5515397</guid>        </item>
        <item>
            <title>Wnt Signaling in Ovarian Development Inhibits Sf1 Activation of Sox9 via the Tesco Enhancer.</title>
            <link>http://www.medworm.com/index.php?rid=5515396&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%3D22128028%26dopt%3DAbstract</link>
            <description>Authors: Bernard P, Ryan J, Sim H, Czech DP, Sinclair AH, Koopman P, Harley VR
    Abstract
    Genome analysis of patients with disorders of sex development, and gain- and loss-of-function studies in mice indicate that gonadal development is regulated by opposing signals. In females, the Wnt/β-catenin canonical pathway blocks testicular differentiation by repressing the expression of the Sertoli cell-specific gene Sox9 by an unknown mechanism. Using cell and embryonic gonad culture models, we show that activation of the Wnt/β-catenin pathway inhibits the expression of Sox9 and Amh, whereas mRNA and protein levels of Sry and steroidogenic factor 1 (Sf1), two key transcriptional regulators of Sox9, are not altered. Ectopic activation of Wnt/β-catenin signaling in male gonads led to a los...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5515396</comments>
            <pubDate>Tue, 29 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5515396</guid>        </item>
        <item>
            <title>A High-Fat Diet Induces Bone Loss in Mice Lacking the Alox5 Gene.</title>
            <link>http://www.medworm.com/index.php?rid=5515395&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%3D22128029%26dopt%3DAbstract</link>
            <description>Authors: Le P, Kawai M, Bornstein S, Demambro VE, Horowitz MC, Rosen CJ
    Abstract
    5-Lipoxygenase catalyzes leukotriene generation from arachidonic acid. The gene that encodes 5-lipoxygenase, Alox5, has been identified in genome-wide association and mouse Quantitative Trait Locus studies as a candidate gene for obesity and low bone mass. Thus, we tested the hypothesis that Alox5(-/-) mice would exhibit metabolic and skeletal changes when challenged by a high-fat diet (HFD). On a regular diet, Alox5(-/-) mice did not differ in total body weight, percent fat mass, or bone mineral density compared with wild-type (WT) controls (P &amp;lt; 0.05). However, when placed on a HFD, Alox5(-/-) gained more fat mass and lost greater areal bone mass vs. WT (P &amp;lt; 0.05). Microarchitectural analyses re...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5515395</comments>
            <pubDate>Tue, 29 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5515395</guid>        </item>
        <item>
            <title>Circadian Regulation of Cortisol Release in Behaviorally Split Golden Hamsters.</title>
            <link>http://www.medworm.com/index.php?rid=5515394&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%3D22128030%26dopt%3DAbstract</link>
            <description>Authors: Lilley TR, Wotus C, Taylor D, Lee JM, de la Iglesia HO
    Abstract
    The master circadian clock located within the hypothalamic suprachiasmatic nucleus (SCN) is necessary for the circadian rhythm of glucocorticoid (GC) release. The pathways by which the SCN sustains rhythmic GC release remain unclear. We studied the circadian regulation of cortisol release in the behaviorally split golden hamster, in which the single bout of circadian locomotor activity splits into two bouts approximately12 h apart after exposing the animals to constant light conditions. We show that unsplit control hamsters present a single peak of cortisol release that is concomitant with a single peak of ACTH release. In contrast, split hamsters show two peaks of cortisol release that are approximately12 h a...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5515394</comments>
            <pubDate>Tue, 29 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5515394</guid>        </item>
        <item>
            <title>GLP-1 Neurons in the Nucleus of the Solitary Tract Project Directly to the Ventral Tegmental Area and Nucleus Accumbens to Control for Food Intake.</title>
            <link>http://www.medworm.com/index.php?rid=5515393&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%3D22128031%26dopt%3DAbstract</link>
            <description>Authors: Alhadeff AL, Rupprecht LE, Hayes MR
    Abstract
    Central glucagon-like-peptide-1 (GLP-1) receptor activation reduces food intake; however, brain nuclei and mechanism(s) mediating this effect remain poorly understood. Although central nervous system GLP-1 is produced almost exclusively in the nucleus of the solitary tract in the hindbrain, GLP-1 receptors (GLP-1R) are expressed throughout the brain, including nuclei in the mesolimbic reward system (MRS), e.g. the ventral tegmental area (VTA) and the nucleus accumbens (NAc). Here, we examine the MRS as a potential site of action for GLP-1-mediated control of food intake and body weight. Double immunohistochemistry for Fluorogold (monosynaptic retrograde tracer) and GLP-1 neuron immunoreactivity indicated that GLP-1-producing nuc...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5515393</comments>
            <pubDate>Tue, 29 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5515393</guid>        </item>
        <item>
            <title>ACTH-Dependent Regulation of MicroRNA As Endogenous Modulators of Glucocorticoid Receptor Expression in the Adrenal Gland.</title>
            <link>http://www.medworm.com/index.php?rid=5515392&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%3D22128032%26dopt%3DAbstract</link>
            <description>Authors: Riester A, Issler O, Spyroglou A, Haramati Rodrig S, Chen A, Beuschlein F
    Abstract
    MicroRNA (miR) are a subset of small RNA molecules, which posttranscriptionally modulate target gene expression. Although miR have been demonstrated to impact a number of processes during development and tumorigenesis, little is known about the expression and the role of miR in the adrenal gland. Because tight regulation of steroid synthesis is crucial for maintaining homeostasis upon stressful stimuli, here, we determined the miR expression pattern in mouse adrenal glands under baseline conditions, as well as 10, 30, and 60 min upon ACTH stimulation, using miR microarray. Changes in miR expression levels detected by array analysis were confirmed by real-time PCR and further analyzed by bioi...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5515392</comments>
            <pubDate>Tue, 29 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5515392</guid>        </item>
        <item>
            <title>Topiramate Treatment Protects Blood-Brain Barrier Pericytes from Hyperglycemia-Induced Oxidative Damage in Diabetic Mice.</title>
            <link>http://www.medworm.com/index.php?rid=5515421&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%3D22109883%26dopt%3DAbstract</link>
            <description>Authors: Price TO, Eranki V, Banks WA, Ercal N, Shah GN
    Abstract
    Diabetes mellitus causes cerebral microvasculature deterioration and cognitive decline. The specialized endothelial cells of cerebral microvasculature comprise the blood-brain barrier, and the pericytes (PC) that are in immediate contact with these endothelial cells are vital for blood-brain barrier integrity. In diabetes, increased mitochondrial oxidative stress is implicated as a mechanism for hyperglycemia-induced PC loss as a prerequisite leading to blood-brain barrier disruption. Mitochondrial carbonic anhydrases (CA) regulate the oxidative metabolism of glucose and thus play an important role in the generation of reactive oxygen species and oxidative stress. We hypothesize that the inhibition of mitochondrial CA...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5515421</comments>
            <pubDate>Tue, 22 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5515421</guid>        </item>
        <item>
            <title>Salt-Inducible Kinase Is Involved in the Regulation of Corticotropin-Releasing Hormone Transcription in Hypothalamic Neurons in Rats.</title>
            <link>http://www.medworm.com/index.php?rid=5515420&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%3D22109884%26dopt%3DAbstract</link>
            <description>Authors: Liu Y, Poon V, Sanchez-Watts G, Watts AG, Takemori H, Aguilera G
    Abstract
    Activation of CRH transcription requires phosphorylation of cAMP response element-binding protein (CREB) and translocation of the CREB coactivator, transducer of regulated CREB activity (TORC) from cytoplasm to nucleus. In basal conditions, transcription is low because TORC remains in the cytoplasm, inactivated by phosphorylation through Ser/Thr protein kinases of the AMP-dependent protein kinases (AMPK) family, including salt-inducible kinase (SIK). To determine which kinase is responsible for TORC phosphorylation in CRH neurons, we measured SIK1 and SIK2 mRNA in the hypothalamic paraventricular nucleus of rats by in situ hybridization. In basal conditions, low mRNA levels of the two kinases were fo...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5515420</comments>
            <pubDate>Tue, 22 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5515420</guid>        </item>
        <item>
            <title>Ubiquitin-Proteasomal Degradation of COX-2 in TGF-β Stimulated Human Endometrial Cells Is Mediated Through Endoplasmic Reticulum Mannosidase I.</title>
            <link>http://www.medworm.com/index.php?rid=5515419&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%3D22109885%26dopt%3DAbstract</link>
            <description>In this study, we investigate the role of TGF-β in the regulation of COX-2 in human uterine stromal cells. Each TGF-β isoform decreases COX-2 protein level in human uterine stromal cells in Smad2/3-dependent manner. The decrease in COX-2 is accompanied by a decrease in PG synthesis. Knockdown of Smad4 using specific small interfering RNA prevents the decrease in COX-2 protein, confirming that Smad pathway is implicated in the regulation of COX-2 expression in human endometrial stromal cells. Pretreatment with 26S proteasome inhibitor, MG132, significantly restores COX-2 protein and PG synthesis, indicating that COX-2 undergoes proteasomal degradation in the presence of TGF-β. In addition, each TGF-β isoform up-regulates endoplasmic reticulum (ER)-mannosidase I (ERManI) implying that CO...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5515419</comments>
            <pubDate>Tue, 22 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5515419</guid>        </item>
        <item>
            <title>Homologous and Heterologous in Vitro Regulation of Pituitary Receptors for Somatostatin, Growth Hormone (GH)-Releasing Hormone, and Ghrelin in a Nonhuman Primate (Papio anubis).</title>
            <link>http://www.medworm.com/index.php?rid=5515418&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%3D22109886%26dopt%3DAbstract</link>
            <description>Authors: Córdoba-Chacón J, Gahete MD, Castaño JP, Kineman RD, Luque RM
    Abstract
    Secretion of GH by pituitary somatotrophs is primarily stimulated by GHRH and ghrelin and inhibited by somatostatin through the activation of specific receptors [GHRH receptor (GHRH-R), GH secretagogue receptor (GHS-R) and somatostatin receptors (sst1-5), respectively]. However, we have shown that somatostatin, at low doses, can also stimulate GH release, directly and specifically, in primary pituitary cultures from a nonhuman primate (baboons, Papio anubis) and pigs. To determine whether somatostatin, GHRH, and ghrelin can also regulate the expression of their receptors in primates, pituitary cultures from baboons were treated for 4 h with GHRH or ghrelin (10(-8) m) or with high (10(-7) m) and low (...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5515418</comments>
            <pubDate>Tue, 22 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5515418</guid>        </item>
        <item>
            <title>The Inhibitory Effects of Neurokinin B on GnRH Pulse Generator Frequency in the Female Rat.</title>
            <link>http://www.medworm.com/index.php?rid=5515417&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%3D22109887%26dopt%3DAbstract</link>
            <description>Authors: Kinsey-Jones JS, Grachev P, Li XF, Lin YS, Milligan SR, Lightman SL, O'Byrne KT
    Abstract
    Neurokinin B (NKB) and its receptor (neurokinin-3 receptor) are coexpressed with kisspeptin and dynorphin A (Dyn) within neurons of the hypothalamic arcuate nucleus, the suggested site of the GnRH pulse generator. It is thought that these neuropeptides interact to regulate gonadotropin secretion. Using the ovariectomized (OVX) and OVX 17β-estradiol-replaced rat models, we have carried out a series of in vivo neuropharmacological and electrophysiological experiments to elucidate the hierarchy between the kisspeptin, NKB, and Dyn signaling systems. Rats were implanted with intracerebroventricular cannulae and cardiac catheters for frequent (every 5 min) automated serial blood sampling. ...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5515417</comments>
            <pubDate>Tue, 22 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5515417</guid>        </item>
        <item>
            <title>Neonatal Exposure to Estradiol/Bisphenol A Alters Promoter Methylation and Expression of Nsbp1 and Hpcal1 Genes and Transcriptional Programs of Dnmt3a/b and Mbd2/4 in the RatProstate Gland Throughout Life.</title>
            <link>http://www.medworm.com/index.php?rid=5515416&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%3D22109888%26dopt%3DAbstract</link>
            <description>Authors: Tang WY, Morey LM, Cheung YY, Birch L, Prins GS, Ho SM
    Abstract
    Evidence supporting an early origin of prostate cancer is growing. We demonstrated previously that brief exposure of neonatal rats to estradiol or bisphenol A elevated their risk of developing precancerous lesions in the prostate upon androgen-supported treatment with estradiol as adults. Epigenetic reprogramming may be a mechanism underlying this inductive event in early life, because we observed overexpression of phosphodiesterase 4D variant 4 (Pde4d4) through induction of hypomethylation of its promoter. This epigenetic mark was invisible in early life (postnatal d 10), becoming apparent only after sexual maturation. Here, we asked whether other estrogen-reprogrammable epigenetic marks have similar or diffe...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5515416</comments>
            <pubDate>Tue, 22 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5515416</guid>        </item>
        <item>
            <title>GH Does Not Modulate the Early Fasting-Induced Release of Free Fatty Acids in Mice.</title>
            <link>http://www.medworm.com/index.php?rid=5515415&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%3D22109889%26dopt%3DAbstract</link>
            <description>Authors: Steyn FJ, Leong JW, Huang L, Tan HY, Xie TY, Nelson C, Waters MJ, Veldhuis JD, Epelbaum J, Chen C
    Abstract
    Fasting results in the mobilization of adipose stores and the elevation of levels of free fatty acids (FFA). In humans, this process is driven by a release in GH. Little is known regarding the role of GH in modulating this process during early stages of fasting in the mouse. Confirmation of the role of GH in modulating FFA release in the fasting mouse is of particular importance given the frequent use of mouse models to study metabolic mechanisms. Here, we correlate the initial release of FFA throughout fasting in mice with pulsatile GH secretion. Observations illustrate the rapid release of FFA in response to food withdrawal. This does not correlate with a rise in GH...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5515415</comments>
            <pubDate>Tue, 22 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5515415</guid>        </item>
        <item>
            <title>TSH Regulates Pendrin Membrane Abundance and Enhances Iodide Efflux in Thyroid Cells.</title>
            <link>http://www.medworm.com/index.php?rid=5515414&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%3D22109890%26dopt%3DAbstract</link>
            <description>Authors: Pesce L, Bizhanova A, Caraballo JC, Westphal W, Butti ML, Comellas A, Kopp P
    Abstract
    Thyroid hormones are essential for normal development and metabolism. Their synthesis requires transport of iodide into thyroid follicles. The mechanisms involving the apical efflux of iodide into the follicular lumen are poorly elucidated. The discovery of mutations in the SLC26A4 gene in patients with Pendred syndrome (congenital deafness, goiter, and defective iodide organification) suggested a possible role for the encoded protein, pendrin, as an apical iodide transporter. We determined whether TSH regulates pendrin abundance at the plasma membrane and whether this influences iodide efflux. Results of immunoblot and immunofluorescence experiments reveal that TSH and forskolin rapidly ...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5515414</comments>
            <pubDate>Tue, 22 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5515414</guid>        </item>
        <item>
            <title>PPARγ Agonist Improves Neuronal Insulin Receptor Function in Hippocampus and Brain Mitochondria Function in Rats with Insulin Resistance Induced by Long Term High-Fat Diets.</title>
            <link>http://www.medworm.com/index.php?rid=5515413&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%3D22109891%26dopt%3DAbstract</link>
            <description>Authors: Pipatpiboon N, Pratchayasakul W, Chattipakorn N, Chattipakorn SC
    Abstract
    We previously demonstrated that a high-fat diet (HFD) consumption can cause not only peripheral insulin resistance, but also neuronal insulin resistance. Moreover, the consumption of an HFD has been shown to cause mitochondrial dysfunction in both the skeletal muscle and liver. Rosiglitazone, a peroxizome proliferator-activated receptor-γ ligand, is a drug used to treat type 2 diabetes mellitus. Recent studies suggested that rosiglitazone can improve learning and memory in both human and animal models. However, the effects of rosiglitazone on neuronal insulin resistance and brain mitochondria after the HFD consumption have not yet been investigated. Therefore, we tested the hypothesis that rosiglita...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5515413</comments>
            <pubDate>Tue, 22 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5515413</guid>        </item>
        <item>
            <title>Increased Numbers of Nonattached Osteoclasts After Long-Term Zoledronic Acid Therapy in Mice.</title>
            <link>http://www.medworm.com/index.php?rid=5515412&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%3D22109892%26dopt%3DAbstract</link>
            <description>In this study, mice received zoledronic acid (ZA) for 13 months, nearly half the lifespan of mice, and the effects of continual osteoclast suppression on the bone environment and oral wound healing were determined. ZA therapy suppressed osteoclasts, resulting in significantly more bone mass compared with control. Despite continuous and intense suppression of bone loss in mice receiving ZA, serum calcium levels were maintained in the normal range. No differences were noted in serum tartrate-resistant acid phosphatase (TRAP) 5b levels between ZA-treated and control mice. Histomorphometric analyses of bones revealed that ZA therapy significantly decreased osteoclasts on the bone surface but, instead, substantially increased TRAP(+) mononuclear cells and osteoclasts that were not on the bone s...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5515412</comments>
            <pubDate>Tue, 22 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5515412</guid>        </item>
        <item>
            <title>Acute Glucocorticoid Administration Rapidly Suppresses Basal and Stress-Induced Hypothalamo-Pituitary-Adrenal Axis Activity.</title>
            <link>http://www.medworm.com/index.php?rid=5426849&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%3D22087024%26dopt%3DAbstract</link>
            <description>Authors: Andrews MH, Wood SA, Windle RJ, Lightman SL, Ingram CD
    Abstract
    Hypothalamo-pituitary-adrenal (HPA) axis activity is subject to negative feedback control by glucocorticoids. Although the rapid component of this feedback is widely considered to contribute to regulation of dynamic HPA activity, few in vivo data exist on the temporal and pharmacological characteristics of this phenomenon. Thus, frequent automated blood sampling was undertaken in rats to determine the effects of acute glucocorticoid administration on basal and stress-induced corticosterone secretion. The glucocorticoid agonist methylprednisolone (5-2000 μg) or dexamethasone (5-500 μg) injected iv at the peak of the diurnal rhythm caused dose-dependent suppression of basal corticosterone secretion, which was ...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5426849</comments>
            <pubDate>Tue, 15 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5426849</guid>        </item>
        <item>
            <title>Cannabinoid Receptor Type 1 (CB1) Activation Inhibits Small GTPase RhoA Activity and Regulates Motility of Prostate Carcinoma Cells.</title>
            <link>http://www.medworm.com/index.php?rid=5426848&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%3D22087025%26dopt%3DAbstract</link>
            <description>In this study, we examined the molecular mechanisms that diminish cell migration upon the CB1 activation in prostate carcinoma cells. The CB1 activation with the agonist WIN55212 significantly diminishes the small GTPase RhoA activity but modestly increases the Rac1 and Cdc42 activity. The diminished RhoA activity is accompanied by the loss of actin/myosin microfilaments, cell spreading, and cell migration. Interestingly, the CB1 inactivation with the selective CB1 antagonist AM251 significantly increases RhoA activity, enhances microfilament formation and cell spreading, and promotes cell migration. This finding suggests that endogenously produced EC activate the CB1, resulting in chronic repression of RhoA activity and cell migration. Consistent with this possibility, RhoA activity is si...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5426848</comments>
            <pubDate>Tue, 15 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5426848</guid>        </item>
        <item>
            <title>Enhanced Thecal Androgen Production Is Prenatally Programmed in an Ovine Model of Polycystic Ovary Syndrome.</title>
            <link>http://www.medworm.com/index.php?rid=5426847&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%3D22087026%26dopt%3DAbstract</link>
            <description>Authors: Hogg K, Young JM, Oliver EM, Souza CJ, McNeilly AS, Colin Duncan W
    Abstract
    One of the hallmarks of polycystic ovary syndrome (PCOS) is increased ovarian androgen secretion that contributes to the ovarian, hormonal, and metabolic features of this condition. Thecal cells from women with PCOS have an enhanced capacity for androgen synthesis. To investigate whether this propensity is a potential cause, rather than a consequence, of PCOS, we used an ovine prenatal androgenization model of PCOS and assessed ewes at 11 months of age. Pregnant Scottish Greyface ewes were administered 100 mg testosterone propionate (TP) or vehicle control twice weekly from d 62 to 102 of gestation, and female offspring (TP = 9, control = 5) were studied. Prenatal TP exposure did not alter ovarian ...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5426847</comments>
            <pubDate>Tue, 15 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5426847</guid>        </item>
        <item>
            <title>The Type 1 Insulin-Like Growth Factor Receptor (IGF-IR) Pathway Is Mandatory For The Follistatin-Induced Skeletal Muscle Hypertrophy.</title>
            <link>http://www.medworm.com/index.php?rid=5426844&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%3D22087027%26dopt%3DAbstract</link>
            <description>In conclusion, the IGF-IR/Akt/mTOR pathway plays a critical role in FS-induced muscle hypertrophy. In contrast, induction of IGF-II expression and S6K activity by FS are not required for the hypertrophic action of FS.
    PMID: 22087027 [PubMed - as supplied by publisher] (Source: Endocrinology)</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5426844</comments>
            <pubDate>Tue, 15 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5426844</guid>        </item>
        <item>
            <title>TGF-β Mediates Suppression of Adipogenesis by Estradiol through Connective Tissue Growth Factor Induction.</title>
            <link>http://www.medworm.com/index.php?rid=5426861&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%3D22067314%26dopt%3DAbstract</link>
            <description>Authors: Kumar A, Ruan M, Clifton K, Syed F, Khosla S, Oursler MJ
    Abstract
    In the bone marrow cavity, adipocyte numbers increase, whereas osteoblast progenitor numbers decrease with aging. Because adipocytes and osteoblasts share a common progenitor, it is possible that this shift is due to an increase in adipocyte-lineage cells at the expense of osteoblast-lineage commitment. Estrogens inhibit adipocyte differentiation, and in both men and women, circulating estrogens correlate with bone loss with aging. In bone cells, estrogens stimulate expression of TGF-β and suppress mesenchymal cell adipogenesis. Using a tripotential mesenchymal cell line, we have examined whether estradiol suppression of adipocyte differentiation is due to stimulation of TGF-β and the mechanism by which TG...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5426861</comments>
            <pubDate>Tue, 08 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5426861</guid>        </item>
        <item>
            <title>Type 2 Corticotropin-Releasing Factor Receptor in the Ventromedial Nucleus of Hypothalamus Is Critical in Regulating Feeding and Lipid Metabolism in White Adipose Tissue.</title>
            <link>http://www.medworm.com/index.php?rid=5426860&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%3D22067315%26dopt%3DAbstract</link>
            <description>Authors: Chao H, Digruccio M, Chen P, Li C
    Abstract
    Ventromedial nucleus of hypothalamus (VMH) plays a critical role in regulating feeding and energy metabolism. The nucleus expresses high levels of the type 2 corticotropin-releasing factor receptor (CRFR2) and receives prominent innervation of nerve fibers containing Urocortin 3 (Ucn 3), an endogenous ligand of the receptor. In the present study, we showed that mice deficient in Ucn 3 had elevated basal feeding and increased nocturnal food intake after overnight fasting compared with the wild-type (WT) littermates. The Ucn 3 null mice also had lower circulating insulin levels compared with those of the WT mice. Interestingly, the mutant mice maintained a comparable body weight with the WT littermates. Mice with reduced CRFR2 expre...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5426860</comments>
            <pubDate>Tue, 08 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5426860</guid>        </item>
        <item>
            <title>Neural Distribution of Vasotocin Receptor mRNA in Two Species of Songbird.</title>
            <link>http://www.medworm.com/index.php?rid=5426859&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%3D22067316%26dopt%3DAbstract</link>
            <description>Authors: Leung CH, Abebe DF, Earp SE, Goode CT, Grozhik AV, Mididoddi P, Maney DL
    Abstract
    The neurohypophyseal hormones vasopressin and oxytocin are produced and released within the mammalian brain, where they act via multiple receptor subtypes. The neural distributions of these receptors, for example, V1a and oxytocin receptors, have been well described in many mammals. In birds, the distribution of binding sites for the homologous neuropeptides, vasotocin (VT) and mesotocin, has been studied in several species by using synthetic radioligands designed to bind to mammalian receptors. Such binding studies, however, may not reveal the specific distributions of each receptor subtype. To identify and map the receptors likely to bind VT and mesotocin, we generated partial cDNA sequence...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5426859</comments>
            <pubDate>Tue, 08 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5426859</guid>        </item>
        <item>
            <title>Lack of Overt FGF21 Resistance in Two Mouse Models of Obesity and Insulin Resistance.</title>
            <link>http://www.medworm.com/index.php?rid=5426858&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%3D22067317%26dopt%3DAbstract</link>
            <description>Authors: Hale C, Chen MM, Stanislaus S, Chinookoswong N, Hager T, Wang M, Véniant MM, Xu J
    Abstract
    Circulating levels of fibroblast growth factor 21 (FGF21), a metabolic regulator of glucose, lipid, and energy homeostasis, are elevated in obese diabetic subjects, raising questions about potential FGF21 resistance. Here we report tissue expression changes in FGF21 and its receptor components, and we describe the target-organ and whole-body responses to FGF21 in ob/ob and diet-induced obese (DIO) mice. Plasma FGF21 concentrations were elevated 8- and 16-fold in DIO and ob/ob mice, respectively, paralleling a dramatic increase in hepatic FGF21 mRNA expression. Concurrently, expression levels of βKlotho, FGF receptor (FGFR)-1c, and FGFR2c were markedly down-regulated in the white ad...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5426858</comments>
            <pubDate>Tue, 08 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5426858</guid>        </item>
        <item>
            <title>11β-Hydroxysteroid Dehydrogenase Type 1, But Not Type 2, Deficiency Worsens Acute Inflammation and Experimental Arthritis in Mice.</title>
            <link>http://www.medworm.com/index.php?rid=5426857&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%3D22067318%26dopt%3DAbstract</link>
            <description>Authors: Coutinho AE, Gray M, Brownstein DG, Salter DM, Sawatzky DA, Clay S, Gilmour JS, Seckl JR, Savill JS, Chapman KE
    Abstract
    Glucocorticoids profoundly influence immune responses, and synthetic glucocorticoids are widely used clinically for their potent antiinflammatory effects. Endogenous glucocorticoid action is modulated by the two isozymes of 11β-hydroxysteroid dehydrogenase (11β-HSD). In vivo, 11β-HSD1 catalyzes the reduction of inactive cortisone or 11-dehydrocorticosterone into active cortisol or corticosterone, respectively, thereby increasing intracellular glucocorticoid levels. 11β-HSD2 catalyzes the reverse reaction, inactivating intracellular glucocorticoids. Both enzymes have been postulated to modulate inflammatory responses. In the K/BxN serum transfer model...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5426857</comments>
            <pubDate>Tue, 08 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5426857</guid>        </item>
        <item>
            <title>Role of IGFBP-3 in the Regulation of β-Cell Mass during Obesity: Adipose Tissue/β-Cell Cross Talk.</title>
            <link>http://www.medworm.com/index.php?rid=5426856&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%3D22067319%26dopt%3DAbstract</link>
            <description>This study analyzed the role of adipose tissue in the control of β-cell replication. Using a diet-induced model of obesity, we obtained conditioned media from three different white adipose tissue depots. Only in the adipose tissue depot surrounding the pancreas did the diet induce changes that led to an increase in INS1E cells and the islet replication rate. To identify the factors responsible for this proliferative effect, adipose tissue gene expression analysis was conducted by microarrays and quantitative RT-PCR. Of all the differentially expressed proteins, only the secreted ones were studied. IGF binding protein 3 (Igfbp3) was identified as the candidate for this effect. Furthermore, in the conditioned media, although the blockage of IGFBP3 led to an increase in the proliferation rat...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5426856</comments>
            <pubDate>Tue, 08 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5426856</guid>        </item>
        <item>
            <title>Identical Gene Regulation Patterns of T3 and Selective Thyroid Hormone Receptor Modulator GC-1.</title>
            <link>http://www.medworm.com/index.php?rid=5426855&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%3D22067320%26dopt%3DAbstract</link>
            <description>Authors: Yuan C, Lin JZ, Sieglaff DH, Ayers SD, Denoto-Reynolds F, Baxter JD, Webb P
    Abstract
    Synthetic selective thyroid hormone (TH) receptor (TR) modulators (STRM) exhibit beneficial effects on dyslipidemias in animals and humans and reduce obesity, fatty liver, and insulin resistance in preclinical animal models. STRM differ from native TH in preferential binding to the TRβ subtype vs. TRα, increased uptake into liver, and reduced uptake into other tissues. However, selective modulators of other nuclear receptors exhibit important gene-selective actions, which are attributed to differential effects on receptor conformation and dynamics and can have profound influences in animals and humans. Although there are suggestions that STRM may exhibit such gene-specific actions, the e...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5426855</comments>
            <pubDate>Tue, 08 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5426855</guid>        </item>
        <item>
            <title>Kisspeptin Signaling Is Indispensable for Neurokinin B, but not Glutamate, Stimulation of Gonadotropin Secretion in Mice.</title>
            <link>http://www.medworm.com/index.php?rid=5426854&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%3D22067321%26dopt%3DAbstract</link>
            <description>We report here a series of neuroendocrine analyses in male mice of a novel Gpr54 knockout (KO) model, generated by heterozygous crossing of a loxP-Gpr54/Protamine-Cre double mutant line. Gpr54-null males showed severe hypogonadotropic hypogonadism but retained robust responsiveness to GnRH. Gonadotropic responses to the agonist of ionotropic glutamate receptors, N-methyl-d-aspartate, were attenuated, but persisted, in Gpr54-null mice. In contrast, LH secretion after activation of metabotropic glutamate receptors was totally preserved in the absence of Gpr54 signaling. Detectable, albeit reduced, LH responses were also observed in Gpr54 KO mice after intracerebroventricular administration of galanin-like peptide or RF9, putative antagonist of neuropeptide FF receptors for the mammalian orth...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5426854</comments>
            <pubDate>Tue, 08 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5426854</guid>        </item>
        <item>
            <title>Prenatal Dexamethasone Exposure Potentiates Diet-Induced Hepatosteatosis and Decreases Plasma IGF-I in a Sex-Specific Fashion.</title>
            <link>http://www.medworm.com/index.php?rid=5426853&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%3D22067322%26dopt%3DAbstract</link>
            <description>In this study, we examined the hypothesis that exposure to the synthetic glucocorticoid, dexamethasone (DEX), during late gestation in the rat results in the development of nonalcoholic fatty liver disease in adult offspring. Pregnant Sprague Dawley dams were treated with 0.4 mg/kg DEX beginning on gestational d 18 until parturition (gestational d 23). At postnatal d 21, offspring were weaned onto either a standard chow or high-fat (60% fat-derived calories) diet. In adulthood (postnatal d 60-65), hepatic tissue was harvested and examined for pathology. Liver steatosis, or fat accumulation, was found to be more severe in the DEX-exposed female offspring that were weaned onto the high-fat diet. This finding corresponded with decreased plasma IGF-I concentrations, as well as decreased hypoth...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5426853</comments>
            <pubDate>Tue, 08 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5426853</guid>        </item>
        <item>
            <title>Mutual Regulation of Growth Hormone and Bone Morphogenetic Protein System in Steroidogenesis by Rat Granulosa Cells.</title>
            <link>http://www.medworm.com/index.php?rid=5426852&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%3D22067323%26dopt%3DAbstract</link>
            <description>In this study, we investigated the actions of GH on steroidogenesis by rat granulosa cells isolated from early antral follicles by focusing on the ovarian bone morphogenetic protein (BMP) system. We found that GH suppressed FSH-induced estradiol production with reduction in aromatase expression and, in contrast, GH increased FSH-induced progesterone level with induction of steroidogenic acute regulatory protein, side chain cleavage cytochrome P450, and 3β-hydroxysteroid dehydrogenase. The effects of GH on steroidogenesis by granulosa cells were enhanced in the presence of the BMP antagonist noggin. Coculture of GH with oocytes did not alter GH regulation of steroidogenesis. Steroid production induced by cAMP donors was not affected by GH treatment and the GH effects on FSH-induced steroid...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5426852</comments>
            <pubDate>Tue, 08 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5426852</guid>        </item>
        <item>
            <title>Constitutive Activation of IKKβ in Adipose Tissue Prevents Diet-Induced Obesity in Mice.</title>
            <link>http://www.medworm.com/index.php?rid=5426851&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%3D22067324%26dopt%3DAbstract</link>
            <description>Authors: Jiao P, Feng B, Ma J, Nie Y, Paul E, Li Y, Xu H
    Abstract
    The IκB kinase β (IKKβ) is a master kinase involved in obesity-related inflammation and insulin resistance through nuclear factor κB dependent and independent pathways. However, the effect of IKKβ activation in adipose tissue, the organ critical for storage of excessive energy and initiation of inflammatory responses in the context of obesity, on systemic insulin sensitivity and metabolism, has not been investigated. In our study, we found that mice overexpressing the constitutively active IKKβ in adipose tissue under the control of murine adipocyte fatty acid binding protein (aP2) promoter were protected from age-related and diet-induced body weight gains, despite increased food intake. The aP2-IKKβ SE mice h...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5426851</comments>
            <pubDate>Tue, 08 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5426851</guid>        </item>
        <item>
            <title>Forkhead Box A1 (FOXA1) and A2 (FOXA2) Oppositely Regulate Human Type 1 Iodothyronine Deiodinase Gene in Liver.</title>
            <link>http://www.medworm.com/index.php?rid=5426850&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%3D22067325%26dopt%3DAbstract</link>
            <description>Authors: Kanamoto N, Tagami T, Ueda-Sakane Y, Sone M, Miura M, Yasoda A, Tamura N, Arai H, Nakao K
    Abstract
    Type 1 iodothyronine deiodinase (D1), a selenoenzyme that catalyzes the bioactivation of thyroid hormone, is expressed mainly in the liver. Its expression and activity are modulated by several factors, but the precise mechanism of its transcriptional regulation remains unclear. In the present study, we have analyzed the promoter of human D1 gene (hDIO1) to identify factors that prevalently increase D1 activity in the human liver. Deletion and mutation analyses demonstrated that a forkhead box (FOX)A binding site and an E-box site within the region between nucleotides -187 and -132 are important for hDIO1 promoter activity in the liver. EMSA demonstrated that FOXA1 and FOXA2 s...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5426850</comments>
            <pubDate>Tue, 08 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5426850</guid>        </item>
        <item>
            <title>Inflammation as a sensor of metabolic stress in obesity and type 2 diabetes.</title>
            <link>http://www.medworm.com/index.php?rid=5382771&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%3D22021196%26dopt%3DAbstract</link>
            <description>Authors: Donath MY
    PMID: 22021196 [PubMed - in process] (Source: Endocrinology)</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5382771</comments>
            <pubDate>Tue, 01 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5382771</guid>        </item>
        <item>
            <title>Sugaring appetite development: mechanisms of neuroendocrine programming.</title>
            <link>http://www.medworm.com/index.php?rid=5382770&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%3D22021197%26dopt%3DAbstract</link>
            <description>Authors: Ozanne SE
    PMID: 22021197 [PubMed - in process] (Source: Endocrinology)</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5382770</comments>
            <pubDate>Tue, 01 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5382770</guid>        </item>
        <item>
            <title>Hagfish, Genome Duplications, and RFamide Neuropeptide Evolution.</title>
            <link>http://www.medworm.com/index.php?rid=5382769&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%3D22021198%26dopt%3DAbstract</link>
            <description>Authors: Dores RM
    PMID: 22021198 [PubMed - in process] (Source: Endocrinology)</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5382769</comments>
            <pubDate>Tue, 01 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5382769</guid>        </item>
        <item>
            <title>Scene of the crime: where is GnRH released, and what might this tell us?</title>
            <link>http://www.medworm.com/index.php?rid=5382768&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%3D22021199%26dopt%3DAbstract</link>
            <description>Authors: Moenter SM
    PMID: 22021199 [PubMed - in process] (Source: Endocrinology)</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5382768</comments>
            <pubDate>Tue, 01 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5382768</guid>        </item>
        <item>
            <title>FGF23 Regulation of Phosphorus Homeostasis Is Dependent on PTH.</title>
            <link>http://www.medworm.com/index.php?rid=5382767&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%3D22021200%26dopt%3DAbstract</link>
            <description>Authors: Clarke BL
    PMID: 22021200 [PubMed - in process] (Source: Endocrinology)</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5382767</comments>
            <pubDate>Tue, 01 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5382767</guid>        </item>
        <item>
            <title>An Irradiation-Altered Bone Marrow Microenvironment Impacts Anabolic Actions of PTH.</title>
            <link>http://www.medworm.com/index.php?rid=5382754&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%3D22045660%26dopt%3DAbstract</link>
            <description>In conclusion, irradiation created a permissive environment for anabolic actions of PTH that was TGFβ dependent but osteoclast independent and suggests that a nonosteoclast source of TGFβ drives mesenchymal stem cell recruitment to support PTH anabolic actions.
    PMID: 22045660 [PubMed - as supplied by publisher] (Source: Endocrinology)</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5382754</comments>
            <pubDate>Tue, 01 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5382754</guid>        </item>
        <item>
            <title>Identification, Expression, and Physiological Functions of Siberian Hamster Gonadotropin-Inhibitory Hormone.</title>
            <link>http://www.medworm.com/index.php?rid=5382753&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%3D22045661%26dopt%3DAbstract</link>
            <description>Authors: Ubuka T, Inoue K, Fukuda Y, Mizuno T, Ukena K, Kriegsfeld LJ, Tsutsui K
    Abstract
    Gonadotropin-inhibitory hormone (GnIH) is a hypothalamic neuropeptide that inhibits gonadotropin secretion in birds and mammals. To further understand its physiological roles in mammalian reproduction, we identified its precursor cDNA and endogenous mature peptides in the Siberian hamster brain. The Siberian hamster GnIH precursor cDNA encoded two RFamide-related peptide (RFRP) sequences. SPAPANKVPHSAANLPLRF-NH(2) (Siberian hamster RFRP-1) and TLSRVPSLPQRF-NH(2) (Siberian hamster RFRP-3) were confirmed as mature endogenous peptides by mass spectrometry from brain samples purified by immunoaffinity chromatography. GnIH mRNA expression was higher in long days (LD) compared with short days (SD). ...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5382753</comments>
            <pubDate>Tue, 01 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5382753</guid>        </item>
        <item>
            <title>Fetal Sex Affects Expression of Renin-Angiotensin System Components in Term Human Decidua.</title>
            <link>http://www.medworm.com/index.php?rid=5382752&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%3D22045662%26dopt%3DAbstract</link>
            <description>Authors: Wang Y, Pringle KG, Sykes SD, Marques FZ, Morris BJ, Zakar T, Lumbers ER
    Abstract
    The maternal decidua expresses the genes of the renin-angiotensin system (RAS). Human decidua was collected at term either before labor (i.e. cesarean delivery) or after spontaneous labor. The mRNA for prorenin (REN), prorenin receptor (ATP6AP2), angiotensinogen (AGT), angiotensin-converting enzymes 1 and 2 (ACE1 and ACE2), angiotensin II type 1 receptor (AGTR1), and angiotensin 1-7 receptor (MAS1) were measured by quantitative real-time RT-PCR. Decidual explants were cultured in duplicate for 24 and 48 h, and all RAS mRNA, and the secretion of prorenin, angiotensin II, and angiotensin 1-7 was measured using quantitative real-time RT-PCR, ELISA, and radioimmunoassay, respectively. In the deci...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5382752</comments>
            <pubDate>Tue, 01 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5382752</guid>        </item>
        <item>
            <title>Spermatogonia Differentiation Requires Retinoic Acid Receptor γ</title>
            <link>http://www.medworm.com/index.php?rid=5382751&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%3D22045663%26dopt%3DAbstract</link>
            <description>Authors: Gely-Pernot A, Raverdeau M, Célébi C, Dennefeld C, Feret B, Klopfenstein M, Yoshida S, Ghyselinck NB, Mark M
    Abstract
    Vitamin A is instrumental to mammalian reproduction. Its metabolite, retinoic acid (RA), acts in a hormone-like manner through binding to and activating three nuclear receptor isotypes, RA receptor (RAR)α (RARA), RARβ, and RARγ (RARG). Here, we show that 1) RARG is expressed by A aligned (A(al)) spermatogonia, as well as during the transition from A(al) to A(1) spermatogonia, which is known to require RA; and 2) ablation of Rarg, either in the whole mouse or specifically in spermatogonia, does not affect meiosis and spermiogenesis but impairs the A(al) to A(1) transition in the course of some of the seminiferous epithelium cycles. Upon ageing, this phe...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5382751</comments>
            <pubDate>Tue, 01 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5382751</guid>        </item>
        <item>
            <title>Stretch and Inflammatory Cytokines Drive Myometrial Chemokine Expression Via NF-κB Activation.</title>
            <link>http://www.medworm.com/index.php?rid=5382750&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%3D22045664%26dopt%3DAbstract</link>
            <description>Authors: Hua R, Pease JE, Sooranna SR, Viney JM, Nelson SM, Myatt L, Bennett PR, Johnson MR
    Abstract
    Both human preterm labor (PTL) and term labor are consistently associated with a chemokine-induced inflammatory infiltration of the myometrium. However, what regulates myometrial chemokine expression and whether the increase in expression precedes the onset of labor, and so may have a role in its causation, or occurs after, and is simply a consequence of labor, is uncertain. Therefore, we assessed 1) chemokine expression in nonlaboring and laboring myometrial samples obtained at and before term and 2) the factors that regulate myometrial chemokine expression. We found that term labor was characterized by an increase in CXCL8 and CCL2 in both upper and lower segments, whereas PTL was...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5382750</comments>
            <pubDate>Tue, 01 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5382750</guid>        </item>
        <item>
            <title>Enhanced Fatty Acid Flux Triggered by Adiponectin Overexpression.</title>
            <link>http://www.medworm.com/index.php?rid=5382749&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%3D22045665%26dopt%3DAbstract</link>
            <description>Authors: Shetty S, Ramos-Roman MA, Cho YR, Brown J, Plutzky J, Muise ES, Horton JD, Scherer PE, Parks EJ
    Abstract
    Adiponectin overexpression in mice increases insulin sensitivity independent of adiposity. Here, we combined stable isotope infusion and in vivo measurements of lipid flux with transcriptomic analysis to characterize fatty acid metabolism in transgenic mice that overexpress adiponectin via the aP2-promoter (ADNTg). Compared with controls, fasted ADNTg mice demonstrated a 31% reduction in plasma free fatty acid concentrations (P = 0.008), a doubling of ketones (P = 0.028), and a 68% increase in free fatty acid turnover in plasma (15.1 ± 1.5 vs. 25.3 ± 6.8 mg/kg · min, P = 0.011). ADNTg mice had 2-fold more brown adipose tissue mass, and triglyceride synthesis and turn...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5382749</comments>
            <pubDate>Tue, 01 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5382749</guid>        </item>
        <item>
            <title>CDH16/Ksp-Cadherin Is Expressed in the Developing Thyroid Gland and Is Strongly Down-Regulated in Thyroid Carcinomas.</title>
            <link>http://www.medworm.com/index.php?rid=5382766&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%3D22028439%26dopt%3DAbstract</link>
            <description>In conclusion, CDH16 is a thyroid-selective and hormone-dependent adhesion protein that might play a role during thyroid development and that may be a useful marker to monitor thyroid carcinomas.
    PMID: 22028439 [PubMed - as supplied by publisher] (Source: Endocrinology)</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5382766</comments>
            <pubDate>Tue, 25 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5382766</guid>        </item>
        <item>
            <title>Activation of Neurokinin 3 Receptors in the Median Preoptic Nucleus Decreases Core Temperature in the Rat.</title>
            <link>http://www.medworm.com/index.php?rid=5382765&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%3D22028440%26dopt%3DAbstract</link>
            <description>Authors: Dacks PA, Krajewski SJ, Rance NE
    Abstract
    Estrogens have pronounced effects on thermoregulation, as illustrated by the occurrence of hot flushes secondary to estrogen withdrawal in menopausal women. Because neurokinin B (NKB) gene expression is markedly increased in the infundibular (arcuate) nucleus of postmenopausal women, and is modulated by estrogen withdrawal and replacement in multiple species, we have hypothesized that NKB neurons could play a role in the generation of flushes. There is no information, however, on whether the primary NKB receptor [neurokinin 3 receptor (NK(3)R)] modulates body temperature in any species. Here, we determine the effects of microinfusion of a selective NK(3)R agonist (senktide) into the rat median preoptic nucleus (MnPO), an important ...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5382765</comments>
            <pubDate>Tue, 25 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5382765</guid>        </item>
        <item>
            <title>Aromatase Deficiency Confers Paradoxical Postischemic Cardioprotection.</title>
            <link>http://www.medworm.com/index.php?rid=5382764&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%3D22028441%26dopt%3DAbstract</link>
            <description>This study's goal was to investigate how aromatase deficiency influences myocardial function and ischemic resilience. RT-PCR analysis of C57Bl/6 mouse hearts confirmed cardiac-specific aromatase expression in adult females. Functional performance of isolated hearts from female aromatase knockout (ArKO) and aromatase wild-type mice were compared. Left ventricular developed pressures were similar in aerobic perfusion, but the maximal rate of rise of ventricular pressure was modestly reduced in ArKO hearts (3725 ± 144 vs. 4272 ± 154 mm Hg/sec, P &amp;lt; 0.05). After 25 min of ischemia, the recovery of left ventricular developed pressure was substantially improved in ArKO (percentage of basal at 60 min of reperfusion, 62 ± 8 vs. 30 ± 6%; P &amp;lt; 0.05). Hypercontracture was attenuated (end dias...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5382764</comments>
            <pubDate>Tue, 25 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5382764</guid>        </item>
        <item>
            <title>Relaxin and Castration in Male Mice Protect from, but Testosterone Exacerbates, Age-Related Cardiac and Renal Fibrosis, Whereas Estrogens Are an Independent Determinant of Organ Size.</title>
            <link>http://www.medworm.com/index.php?rid=5382763&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%3D22028442%26dopt%3DAbstract</link>
            <description>This study determined the effects of castration and hormone replacement therapy on the age-related cardiac and renal pathology of male relaxin gene-knockout (RlnKO) and age-matched wild-type (RlnWT) mice and that of aged male aromatase knockout (ArKO) mice, which lack estrogens and have 5-10 times the androgen levels of male wild-type mice. One-month-old RlnWT and RlnKO mice were bilaterally gonadectomized or sham operated and maintained until 12 months. Subgroups of castrated animals received testosterone or 17β-estradiol treatment from 9 to 12 months. Male ArKO mice and aromatase wild-type mice were aged to 12 months. Collected heart and kidney tissues were assessed for changes in organ size and fibrosis. Castration reduced body, heart, left ventricle, and kidney weights in both RlnKO a...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5382763</comments>
            <pubDate>Tue, 25 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5382763</guid>        </item>
        <item>
            <title>Neurotrophins Acting Via TRKB Receptors Activate the JAGGED1-NOTCH2 Cell-Cell Communication Pathway to Facilitate Early Ovarian Development.</title>
            <link>http://www.medworm.com/index.php?rid=5382762&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%3D22028443%26dopt%3DAbstract</link>
            <description>Authors: Dorfman MD, Kerr B, Garcia-Rudaz C, Paredes AH, Dissen GA, Ojeda SR
    Abstract
    Tropomyosin-related kinase (TRK) receptor B (TRKB) mediates the supportive actions of neurotrophin 4/5 and brain-derived neurotrophic factor on early ovarian follicle development. Absence of TRKB receptors reduces granulosa cell (GC) proliferation and delays follicle growth. In the present study, we offer mechanistic insights into this phenomenon. DNA array and quantitative PCR analysis of ovaries from TrkB-null mice revealed that by the end of the first week of postnatal life, Jagged1, Hes1, and Hey2 mRNA abundance is reduced in the absence of TRKB receptors. Although Jagged1 encodes a NOTCH receptor ligand, Hes1 and Hey2 are downstream targets of the JAGGED1-NOTCH2 signaling system. Jagged1 is p...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5382762</comments>
            <pubDate>Tue, 25 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5382762</guid>        </item>
        <item>
            <title>Effects of Manipulating Hypothalamic Triiodothyronine Concentrations on Seasonal Body Weight and Torpor Cycles in Siberian Hamsters.</title>
            <link>http://www.medworm.com/index.php?rid=5382761&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%3D22028444%26dopt%3DAbstract</link>
            <description>Authors: Murphy M, Jethwa PH, Warner A, Barrett P, Nilaweera KN, Brameld JM, Ebling FJ
    Abstract
    Siberian hamsters display photoperiodically regulated annual cycles in body weight, appetite, and reproduction. Previous studies have revealed a profound up-regulation of type 3 deiodinase (DIO3) mRNA in the ventral ependyma of the hypothalamus associated with hypophagia and weight loss in short-day photoperiods. DIO3 reduces the local availability of T(3), so the aim of this study was to test the hypothesis that decreased hypothalamic T(3) availability underlies the short-day-induced catabolic state. The experimental approach was to determine whether a local increase in T(3) in the hypothalamus of hamsters exposed to short days could reverse the behavioral and physiological changes indu...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5382761</comments>
            <pubDate>Tue, 25 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5382761</guid>        </item>
        <item>
            <title>Endothelial Dysfunction in a Rat Model of PCOS: Evidence of Increased Vasoconstrictor Prostanoid Activity.</title>
            <link>http://www.medworm.com/index.php?rid=5382760&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%3D22028445%26dopt%3DAbstract</link>
            <description>Authors: Keller J, Mandala M, Casson P, Osol G
    Abstract
    Clinical research demonstrates an association between polycystic ovary syndrome (PCOS) and endothelial dysfunction, a pathological state widely believed to be a hallmark of vascular disease; the underlying pathways, however, have not been defined. The purpose of this study was to characterize endothelial function in resistance arteries in a novel rat model of PCOS. Female rats were randomized at 3-4 wk to implantation of a 7.5-mg, 90-d dihydrotestosterone (DHT) pellet or a matched placebo. At 15-16 wk, experiments were performed on isolated mesenteric resistance arteries using a pressurized arteriograph. Endothelial function was assessed by the vasodilatory response of preconstricted arteries to acetylcholine (ACh) in the abse...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5382760</comments>
            <pubDate>Tue, 25 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5382760</guid>        </item>
        <item>
            <title>Analysis of Fertility-Related Soluble Mediators in Human Uterine Fluid Identifies VEGF as a Key Regulator of Embryo Implantation.</title>
            <link>http://www.medworm.com/index.php?rid=5382759&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%3D22028446%26dopt%3DAbstract</link>
            <description>This study aimed first to identify the growth factor and cytokine profile of human uterine fluid from fertile women during the midproliferative (MP; nonreceptive) and MS (receptive) phases of the cycle, and from women with unexplained infertility during the MS phase. The second aim was to determine important functions of endometrial secretions for embryo implantation. Analysis of uterine fluid using quantitative Luminex assays revealed the presence of over 30 cytokines and growth factors, of which eight [platelet-derived growth factor-AA, TNF-B, soluble IL-2 receptor-A, Fms-like tyrosine kinase 3 ligand, soluble CD40 ligand, IL-7, interferon-A2, and chemokine (C-X-C motif) ligand 1-3] were previously unknown in human uterine fluid. Comparison of the fertile MP, MS, and infertile MS cohorts...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5382759</comments>
            <pubDate>Tue, 25 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5382759</guid>        </item>
        <item>
            <title>Heparin-Binding EGF-Like Growth Factor (HB-EGF) Mediates 5-HT-Induced Insulin Resistance Through Activation of EGF Receptor-ERK1/2-mTOR Pathway.</title>
            <link>http://www.medworm.com/index.php?rid=5382758&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%3D22028447%26dopt%3DAbstract</link>
            <description>In this report, we provide evidence that 5-HT induced production of heparin-binding epidermal growth factor-like growth factor (HB-EGF) and caused insulin resistance in 3T3-L1 adipocytes, primary adipocytes, and C2C12 myotubes. In 3T3-L1 adipocytes, 5-HT stimulated HB-EGF production by promoting metalloproteinase-dependent shedding of transmembrane protein pro-HB-EGF. HB-EGF then bound and tyrosine-phosphorylated EGF receptors, which activated the mammalian target of rapamycin pathway through ERK1/2 phosphorylation. Mammalian target of rapamycin activation caused serine phosphorylation of insulin receptor substrate-1, which attenuated insulin-stimulated tyrosine phosphorylation of insulin receptor substrate-1 and glucose uptake. Pharmacological inhibition of either Gq/11-coupled receptors ...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5382758</comments>
            <pubDate>Tue, 25 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5382758</guid>        </item>
        <item>
            <title>Inherent Growth Hormone Resistance in the Skeletal Muscle of the Fine Flounder Is Modulated by Nutritional Status and Is Characterized by High Contents of Truncated GHR, Impairment in the JAK2/STAT5 Signaling Pathway, and Low IGF-I Expression.</title>
            <link>http://www.medworm.com/index.php?rid=5382757&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%3D22028448%26dopt%3DAbstract</link>
            <description>Authors: Fuentes EN, Einarsdottir IE, Valdes JA, Alvarez M, Molina A, Björnsson BT
    Abstract
    A detailed understanding of how the GH and IGF-I regulate muscle growth, especially in early vertebrates, is still lacking. The fine flounder is a flatfish species exhibiting remarkably slow growth, representing an intriguing model for elucidating growth regulatory mechanisms. Key components of the GH system were examined in groups of fish during periods of feeding, fasting, and refeeding. Under feeding conditions, there is an inherent systemic and local (muscle) GH resistance, characterized by higher levels of plasma GH than of IGF-I, skeletal muscle with a greater content of the truncated GH receptor (GHRt) than of full-length GHR (GHRfl), an impaired activation of the Janus kinase 2 (JAK...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5382757</comments>
            <pubDate>Tue, 25 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5382757</guid>        </item>
        <item>
            <title>Minireview: Recent Advances in Extranuclear Steroid Receptor Actions.</title>
            <link>http://www.medworm.com/index.php?rid=5382756&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%3D22028449%26dopt%3DAbstract</link>
            <description>Authors: Hammes SR, Levin ER
    Abstract
    The participation of extranuclear steroid receptor signaling in organ physiology and the impact for pathobiology has increasingly been demonstrated. Important functions of membrane estrogen receptors in the cardiovascular system demonstrate new mechanisms of rapid steroid signaling to gene regulation, preventing cardiovascular disease and maintaining healthy arterial function. In cancer cells, kinase signaling initiated by extranuclear estrogen, progesterone, and androgen receptors modulates transcriptional events in the nucleus, which in turn regulate proliferation, migration, and invasion. Important mediators of cross talk between cytoplasmic and nuclear steroid receptor signaling are the proline-, glutamic acid-, and leucine-rich protein-1 a...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5382756</comments>
            <pubDate>Tue, 25 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5382756</guid>        </item>
        <item>
            <title>Noninvasive Analytical Estimation of Endogenous GnRH Drive: Analysis Using Graded Competitive GnRH-Receptor Antagonism and a Calibrating Pulse of Exogenous GnRH.</title>
            <link>http://www.medworm.com/index.php?rid=5382755&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%3D22028450%26dopt%3DAbstract</link>
            <description>Authors: Keenan DM, Clarke IJ, Veldhuis JD
    Abstract
    Homeostatic control of endocrine systems proceeds via feedforward (agonistic, stimulatory) and feedback (antagonistic, inhibitory) interactions mediated via implicit dose-response functions. However, neither the feedback/feedforward pathways nor the dose-response interfaces are directly observed in vivo. Thus, the goal was to formulate and estimate an ensemble construct of time-varying feedback/feedforward interactions among GnRH, LH, and testosterone (T) in the male gonadal axis. The new analytical model revises and extends an earlier construct by: 1) allowing systemic T concentrations to inhibit hypothalamic GnRH output; 2) estimating GnRH outflow after injection of a calibrating pulse of biosynthetic GnRH; 3) framing the pituit...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5382755</comments>
            <pubDate>Tue, 25 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5382755</guid>        </item>
        <item>
            <title>Dietary Phosphate Restriction Normalizes Biochemical and Skeletal Abnormalities in a Murine Model of Tumoral Calcinosis.</title>
            <link>http://www.medworm.com/index.php?rid=5382779&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%3D22009723%26dopt%3DAbstract</link>
            <description>In conclusion, dietary phosphate restriction normalizes biochemical and skeletal phenotypes of Galnt3 knockout mice and, thus, can be an effective therapy for tumoral calcinosis.
    PMID: 22009723 [PubMed - as supplied by publisher] (Source: Endocrinology)</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5382779</comments>
            <pubDate>Tue, 18 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5382779</guid>        </item>
        <item>
            <title>Heparanase Is Highly Expressed and Regulates Proliferation in GH-Secreting Pituitary Tumor Cells.</title>
            <link>http://www.medworm.com/index.php?rid=5382778&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%3D22009724%26dopt%3DAbstract</link>
            <description>Authors: Rubinfeld H, Cohen-Kaplan V, Nass D, Ilan N, Meisel S, Cohen ZR, Hadani M, Vlodavsky I, Shimon I
    Abstract
    Pituitary tumorigenesis involves remodeling of the extracellular matrix (ECM). Heparanase, an endoglycosidase capable of degrading heparan sulfate, a major polysaccharide constituent of the ECM, is implicated in diverse processes associated with ECM remodeling, such as morphogenesis, angiogenesis, and tumor invasion. The aim of this study was to investigate the possible role of heparanase in pituitary tumorigenesis. Human normal pituitaries and pituitary tumors were examined for heparanase mRNA and protein expression using real-time PCR and immunohistochemistry, respectively. Cell proliferation was assessed by colony formation after heparanase overexpression in GH3 and...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5382778</comments>
            <pubDate>Tue, 18 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5382778</guid>        </item>
        <item>
            <title>Catechol-O-Methyltransferase Is Dispensable for Vascular Protection by Estradiol in Mouse Models of Atherosclerosis and Neointima Formation.</title>
            <link>http://www.medworm.com/index.php?rid=5382777&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%3D22009725%26dopt%3DAbstract</link>
            <description>In conclusion, the COMT enzyme is dispensable for vascular protection by exogenous estradiol in experimental atherosclerosis and neointima formation in vivo. Instead, COMT deficiency in virgin female mice with intact endogenous production of estradiol results in relative protection against atherosclerosis.
    PMID: 22009725 [PubMed - as supplied by publisher] (Source: Endocrinology)</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5382777</comments>
            <pubDate>Tue, 18 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5382777</guid>        </item>
        <item>
            <title>17{beta}-Estradiol Protects the Lung against Acute Injury: Possible Mediation by Vasoactive Intestinal Polypeptide.</title>
            <link>http://www.medworm.com/index.php?rid=5382776&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%3D22009726%26dopt%3DAbstract</link>
            <description>Authors: Hamidi SA, Dickman KG, Berisha H, Said SI
    Abstract
    Beyond their classical role as a class of female sex hormones, estrogens (e.g. 17β-estradiol) exert important biological actions, both protective and undesirable. We have investigated the ability of estradiol to protect the lung in three models of acute injury induced by 1) oxidant stress due to the herbicide paraquat; 2) excitotoxicity, caused by glutamate agonist N-methyl-d-aspartate; and 3) acute alveolar anoxia. We also assessed the role of estrogen receptors (ER) ERα and ERβ and the neuropeptide vasoactive intestinal peptide (VIP) in mediating this protection. Isolated guinea pig or rat lungs were perfused in situ at constant flow and mechanically ventilated. The onset and severity of lung injury were monitored by ...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5382776</comments>
            <pubDate>Tue, 18 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5382776</guid>        </item>
        <item>
            <title>Role of Substance P in the Regulation of Glucose Metabolism via Insulin Signaling-Associated Pathways.</title>
            <link>http://www.medworm.com/index.php?rid=5382775&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%3D22009727%26dopt%3DAbstract</link>
            <description>Authors: Karagiannides I, Bakirtzi K, Kokkotou E, Stavrakis D, Gross Margolis K, Thomou T, Giorgadze N, Kirkland JL, Pothoulakis C
    Abstract
    Substance P (SP), encoded by the tachykinin 1 (Tac1) gene, is the most potent tachykinin ligand for the high-affinity neurokinin-1 receptor (NK-1R). We previously reported that NK-1R-deficient mice show less weight gain and reduced circulating levels of leptin and insulin in response to a high-fat diet (HFD) and demonstrated the presence of functional NK-1R in isolated human preadipocytes. Here we assessed the effects of SP on weight gain in response to HFD and determined glucose metabolism in Tac1-deficient (Tac1(-/-)) mice. The effect of SP on the expression of molecules that may predispose to reduced glucose uptake was also determined in iso...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5382775</comments>
            <pubDate>Tue, 18 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5382775</guid>        </item>
        <item>
            <title>Angiotensin II Signaling Promotes Follicle Growth and Dominance in Cattle.</title>
            <link>http://www.medworm.com/index.php?rid=5382774&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%3D22009728%26dopt%3DAbstract</link>
            <description>In conclusion, these data suggest that AngII signaling promotes follicle growth in cattle and does so by regulating genes involved in estradiol secretion and granulosa cell proliferation and differentiation.
    PMID: 22009728 [PubMed - as supplied by publisher] (Source: Endocrinology)</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5382774</comments>
            <pubDate>Tue, 18 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5382774</guid>        </item>
        <item>
            <title>Developmental Programming: Gestational Testosterone Treatment Alters Fetal Ovarian Gene Expression.</title>
            <link>http://www.medworm.com/index.php?rid=5382773&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%3D22009729%26dopt%3DAbstract</link>
            <description>This study addresses whether expression of key ovarian genes and microRNA are altered by prenatal T excess and whether changes are mediated by androgenic or estrogenic actions of T. Pregnant Suffolk ewes were treated with T or T plus the androgen receptor antagonist, flutamide (T+F) from d 30 to 90 of gestation. Expression of steroidogenic enzymes, steroid/gonadotropin receptors, and key ovarian regulators were measured by RT-PCR using RNA obtained from fetal ovaries collected on d 65 [n = 4, 5, and 5 for T, T+F, and control groups, respectively] and d 90 (n = 5, 7, 4) of gestation. Additionally, fetal d 90 RNA were hybridized to multispecies microRNA microarrays. Prenatal T decreased (P &amp;lt; 0.05) Cyp11a1 expression (3.7-fold) in d 90 ovaries and increased Cyp19 (3.9-fold) and 5α-reducta...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5382773</comments>
            <pubDate>Tue, 18 Oct 2011 04:00:00 +0100</pubDate>
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            <title>The Osteoclast-Associated Receptor (OSCAR) Is a Novel Receptor Regulated by Oxidized Low-Density Lipoprotein in Human Endothelial Cells.</title>
            <link>http://www.medworm.com/index.php?rid=5382772&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%3D22009730%26dopt%3DAbstract</link>
            <description>Authors: Goettsch C, Rauner M, Sinningen K, Helas S, Al-Fakhri N, Nemeth K, Hamann C, Kopprasch S, Aikawa E, Bornstein SR, Schoppet M, Hofbauer LC
    Abstract
    Cross talks between the vascular and immune system play a critical role in vascular diseases, in particular in atherosclerosis. The osteoclast-associated receptor (OSCAR) is a regulator of osteoclast differentiation and dendritic cell maturation. Whether OSCAR plays a role in vascular biology and has an impact on atherogenic processes provoked by proinflammatory stimuli is yet unknown. We identified OSCAR on the surface of human primary endothelial cells. Stimulation of endothelial cells with oxidized low-density lipoprotein (oxLDL) caused a time- and dose-dependent induction of OSCAR, which was lectin-like oxidized LDL receptor...</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5382772</comments>
            <pubDate>Tue, 18 Oct 2011 04:00:00 +0100</pubDate>
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            <title>Lipopolysaccharide Initiates Inflammation in Bovine Granulosa Cells via the TLR4 Pathway and Perturbs Oocyte Meiotic Progression in Vitro.</title>
            <link>http://www.medworm.com/index.php?rid=5382789&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%3D21990308%26dopt%3DAbstract</link>
            <description>In conclusion, bovine granulosa cells initiate an innate immune response to LPS via the TLR4 pathway, leading to inflammation and to perturbation of meiotic competence.
    PMID: 21990308 [PubMed - as supplied by publisher] (Source: Endocrinology)</description>
            <author>Endocrinology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5382789</comments>
            <pubDate>Tue, 11 Oct 2011 04:00:00 +0100</pubDate>
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