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        <title>Am J Physiol Endocri... 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 'Am J Physiol Endocri...' source.</description>
        <link><![CDATA[http://www.medworm.com/rss/search.php?qu=Am+J+Physiol+Endocri...&t=Am+J+Physiol+Endocri...&s=Search&f=source]]></link>
        <lastBuildDate>Sat, 20 Mar 2010 14:12:53 +0100</lastBuildDate>
        <item>
            <title>Exendin-4 increases blood glucose levels acutely in rats by activation of the sympathetic nervous system.</title>
            <link>http://www.medworm.com/index.php?rid=3332059&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20197503%26dopt%3DAbstract</link>
            <description>Authors: Perez-Tilve D, Gonz&amp;#xE1;lez-Mat&amp;#xED;as LC, Aulinger BA, Alvarez-Crespo M, Gil-Lozano M, Alvarez E, Andrade MA, Tschoep MH, D'Alessio D, Mallo F
    Exendin-4 (Ex-4), an agonist of the glucagon-like peptide-1 receptor (GLP-1r), shares many of the actions of GLP-1 on pancreatic islets, the central nervous system and the gastrointestinal tract that mediate glucose homeostasis and food intake. Because Ex-4 has a much longer plasma half-life than GLP-1, it is an effective drug for reducing blood glucose levels in patients with type 2 diabetes mellitus (T2DM). Here we report that acute administration of Ex-4, in relatively high doses, either into the peripheral circulation or the CNS, paradoxically increased blood glucose levels in rats. This effect was independent of the insulinotrop...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3332059</comments>
            <pubDate>Tue, 02 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3332059</guid>        </item>
        <item>
            <title>ADIPONECTIN DIMINISHES PLATELET AGGREGATION AND sCD40L RELEASE. POTENTIAL ROLE IN THE METABOLIC SYNDROME.</title>
            <link>http://www.medworm.com/index.php?rid=3332058&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20197504%26dopt%3DAbstract</link>
            <description>Conclusions: Enhanced platelet aggregation and activation markers are found in the metabolic syndrome associated to low adiponectin concentrations. Novel evidence is provided demonstrating that adiponectin has anti-thrombotic properties, since it inhibits platelet aggregation and platelet activation.
    PMID: 20197504 [PubMed - as supplied by publisher] (Source: Am J Physiol Endocri...)</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3332058</comments>
            <pubDate>Tue, 02 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3332058</guid>        </item>
        <item>
            <title>17{beta}-Estradiol modulates the macrophage migration inhibitory factor secretory pathway by regulating ABCA1 expression in human first-trimester placenta.</title>
            <link>http://www.medworm.com/index.php?rid=3298840&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20173014%26dopt%3DAbstract</link>
            <description>Authors: Ietta F, Bechi N, Romagnoli R, Bhattacharjee J, Realacci M, Di Vito M, Ferretti C, Paulesu L
    Successful pregnancy involves a series of events, most of them mediated by hormones and cytokines. Estrogens, besides being important for placental growth and embryo development, have a marked effect on the immune system exerting either pro- or anti-inflammatory properties. Numerous studies suggest that estrogens directly affect cellular function, including cytokine production. Macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine involved in pregnancy, particularly during the earlier stages of placentation. Since reports on mice have shown that estrogens modulate MIF, herein we investigated the effect of estrogens on human placental MIF. By using an in vitro model...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3298840</comments>
            <pubDate>Tue, 23 Feb 2010 20:26:06 +0100</pubDate>
            <guid isPermaLink="false">3298840</guid>        </item>
        <item>
            <title>Overexpression of nuclear receptor SHP in adipose tissues affects diet-induced obesity and adaptive thermogenesis.</title>
            <link>http://www.medworm.com/index.php?rid=3240220&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20124506%26dopt%3DAbstract</link>
            <description>In conclusion, SHP activation in adipocytes strongly affects weight gain and diet-induced obesity. Developing synthetic compound to antagonize the effect of SHP may prove to be useful in treating obesity.
    PMID: 20124506 [PubMed - as supplied by publisher] (Source: Am J Physiol Endocri...)</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3240220</comments>
            <pubDate>Tue, 02 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3240220</guid>        </item>
        <item>
            <title>eNOS plays a major role in adiponectin synthesis in adipocytes.</title>
            <link>http://www.medworm.com/index.php?rid=3240219&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20124507%26dopt%3DAbstract</link>
            <description>This study was undertaken to test the hypothesis that endothelial NO synthase (eNOS) plays an important role in adiponectin synthesis by producing NO and enhancing mitochondrial function in adipocytes. We examined the effects of eNOS knockdown on adiponectin synthesis in 3T3L1 adipocytes, and also examined plasma adiponectin levels and the mitochondria in adipose tissue of eNOS knockout (eNOS(-/-)) mice with and without chronic administration of a NO donor. In cultured 3T3L1 adipocytes, eNOS siRNA decreased rosiglitazone-induced adiponectin secretion, which was associated with decreases in mitochondrial proteins and biogenesis factors. Plasma adiponectin concentrations were reduced in adult eNOS(-/-) mice, compared to age-matched wild-type mice. Mitochondrial contents in adipose tissue wer...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3240219</comments>
            <pubDate>Tue, 02 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3240219</guid>        </item>
        <item>
            <title>Insulin attenuates myocardial ischemia/reperfusion injury via reducing oxidative/nitrative stress.</title>
            <link>http://www.medworm.com/index.php?rid=3240218&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20124508%26dopt%3DAbstract</link>
            <description>Conclusions: Insulin exerts cardioprotective effect against MI/R injury by blocking ONOO(-) formation. Increased physiological NO production (via eNOS phosphorylation) and superoxide anion reduction contribute to the antioxidative/antinitrative effect of insulin, which can be reversed by inhibiting PI3 Kinase. These results provide important novel information on the mechanisms of cardiovascular actions of insulin.
    PMID: 20124508 [PubMed - as supplied by publisher] (Source: Am J Physiol Endocri...)</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3240218</comments>
            <pubDate>Tue, 02 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3240218</guid>        </item>
        <item>
            <title>IVGTT Glucose Minimal Model Covariate Selection by NonLinear Mixed-Effects Approach.</title>
            <link>http://www.medworm.com/index.php?rid=3215145&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20103736%26dopt%3DAbstract</link>
            <description>Authors: Denti P, Bertoldo A, Vicini P, Cobelli C
    Population approaches, traditionally employed in pharmacokinetic-pharmacodynamic studies, have shown value also in the context of glucose-insulin metabolism models, by providing more accurate individual parameters estimates and a compelling statistical framework for the analysis of between-subject variability (BSV). In this work, the advantages of population techniques are further explored by proposing integration of covariates in the intravenous glucose tolerance test (IVGTT) glucose minimal model analysis. A previously published dataset of 204 healthy subjects, who underwent insulin-modified IVGTTs, was analyzed in NONMEM, and relevant demographic information about each subject were employed to explain part of BSV observed in paramete...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3215145</comments>
            <pubDate>Tue, 26 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3215145</guid>        </item>
        <item>
            <title>AMPK and SIRT1: A Longstanding Partnership?</title>
            <link>http://www.medworm.com/index.php?rid=3215144&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20103737%26dopt%3DAbstract</link>
            <description>Authors: Ruderman NB, Xu XJ, Nelson LE, Cacicedo JM, Saha AK, Lan F, Ido Y
    AMPK activated protein kinase (AMPK) and the histone/protein deacetylase SIRT1 are fuel sensing molecules that have co-existed in cells throughout evolution. When a cell's energy state is diminished, AMPK activation restores energy balance by stimulating catabolic processes that generate ATP and downregulating anabolic processes that consume ATP, but are not acutely needed for survival. SIRT1 in turn is best known historically for producing genetic changes that mediate the increase in longevity caused by calorie restriction. Although the two molecules have been intensively studied for many years, only recently has it become apparent that they have similar effects on such diverse processes as cellular fuel metabo...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3215144</comments>
            <pubDate>Tue, 26 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3215144</guid>        </item>
        <item>
            <title>Treatment with an ssri antidepressant restores hippocampo-hypothalamic corticosteroid feedback and reverses insulin resistance in low birth weight rats.</title>
            <link>http://www.medworm.com/index.php?rid=3215143&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20103738%26dopt%3DAbstract</link>
            <description>Conclusion: These data suggest that the insulin resistance and chronic HPA-axis hyperactivity in LBW rats can be reversed by treatment with an ESC, which down-regulates HPA-axis activity, lowers glucocorticoid exposure and restores insulin sensitivity in LBW rats.
    PMID: 20103738 [PubMed - as supplied by publisher] (Source: Am J Physiol Endocri...)</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3215143</comments>
            <pubDate>Tue, 26 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3215143</guid>        </item>
        <item>
            <title>PDK1/ FoxO1 pathway in POMC neurons regulates Pomc expression and food intake.</title>
            <link>http://www.medworm.com/index.php?rid=3215142&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20103739%26dopt%3DAbstract</link>
            <description>Authors: Iskandar K, Cao Y, Hayashi Y, Nakata M, Takano E, Yada T, Zhang C, Ogawa W, Oki M, Chua S, Itoh H, Noda T, Kasuga M, Nakae J
    Both insulin and leptin signaling converge on phosphatidylinositol-3-OH kinase (PI(3)K)/3-Phosphoinositide-Dependent Protein Kinase 1 (PDK1)/protein kinase B (PKB, also known Akt) in Pro-opiomelanocortin (POMC) neurons. Forkhead box-containing protein O (FoxO) 1 is inactivated in a PI(3)K-dependent manner. However, the interrelationship between PI(3)K/PDK1/Akt and FoxO1 and the chronic effects of the overexpression of FoxO1 in POMC neurons on energy homeostasis has not been elucidated. To determine the extent to which PDK1 and FoxO1 signaling in POMC neurons was responsible for energy homeostasis, we generated POMC neuron-specific Pdk1 knockout mice (POM...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3215142</comments>
            <pubDate>Tue, 26 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3215142</guid>        </item>
        <item>
            <title>HOXA10 Regulates Endometrial GABAA {pi} Receptor Expression and Membrane Translocation.</title>
            <link>http://www.medworm.com/index.php?rid=3215141&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20103740%26dopt%3DAbstract</link>
            <description>Authors: Sadeghi H, Taylor HS
    Expression of the GABA(A) pi receptor has been previously described in the human endometrium in both luminal epithelium and stroma. Its expression is increased during decidualization in rodents and in the implantation window of human endometrium. Here we localized GABA pi subunit receptor protein in human endometrium and identified regulators of gene expression and activation. GABA(A) pi was localized to the cell surface and expression increased during the window of embryo implantation in human endometrium. The well-differentiated human endometrial adenocarcinoma cell line Ishikawa was treated with progesterone, transfected with pcDNA/HOXA10, HOXA10 siRNA or respective controls. GABA(A) pi receptor mRNA expression was evaluated by real time RT-PCR. Protein...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3215141</comments>
            <pubDate>Tue, 26 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3215141</guid>        </item>
        <item>
            <title>Shedding light on the enigma of myocardial lipotoxicity: The involvement of known and putative regulators of fatty acid storage and mobilization.</title>
            <link>http://www.medworm.com/index.php?rid=3215140&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20103741%26dopt%3DAbstract</link>
            <description>Authors: Brindley DN, Kok BP, Kienesberger PC, Lehner R, Dyck JR
    Brindley DN, Kok BPC, Kienesberger PC, Richard Lehner R, Dyck JRB. Excessive fatty acid (FA) uptake by cardiac myocytes is often associated with adverse changes in cardiac function. This is especially evident in diabetic individuals where increased intra-myocardial triacylglycerol (TG) resulting from the exposure to high levels of circulating FA has been proposed to be a major contributor to diabetic cardiomyopathy. At present, our knowledge of how the heart regulates FA storage in TG and the hydrolysis of this TG is limited. This review will concentrate on what is known about TG turnover within the heart and how this is likely to be regulated by extrapolating results from other tissues. We will also assess the evidence a...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3215140</comments>
            <pubDate>Tue, 26 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3215140</guid>        </item>
        <item>
            <title>Placental expression of myostatin and follistatin like-3 protein in a model of developmental programming.</title>
            <link>http://www.medworm.com/index.php?rid=3215139&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20103742%26dopt%3DAbstract</link>
            <description>Authors: Peiris HN, Ponnampalam AP, Osepchook CC, Mitchell MD, Green MP
    Maternal under-nutrition during gestation is known to be detrimental to fetal development, leading to a propensity for metabolic disorders later in the adult lives of the offspring. Identifying possible mediators and physiological processes involved in modulating nutrient transport within the placenta are essential in order to prevent and/or develop treatments for the effects of aberrant nutrition, nutrient transfer and detrimental changes to fetal development. A potential role for myostatin, as a mediator of nutrient uptake and transport from the mother to the fetus, was shown through the recent finding that myostatin acts within the human placenta to modulate glucose uptake and therefore homeostasis. The mRNA and...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3215139</comments>
            <pubDate>Tue, 26 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3215139</guid>        </item>
        <item>
            <title>Dihydrotestosterone Alters Cyclooxygenase-2 Levels in Human Coronary Artery Smooth Muscle Cells.</title>
            <link>http://www.medworm.com/index.php?rid=3215138&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20103743%26dopt%3DAbstract</link>
            <description>Authors: Osterlund KL, Handa RJ, Gonzales RJ
    Both protective and non-protective effects of androgens on the cardiovascular system have been reported. Our previous studies show that the potent androgen receptor (AR) agonist dihydrotestosterone (DHT) increases levels of the vascular inflammatory mediator cyclooxygenase-2 (COX-2) in rodent cerebral arteries independent of any inflammatory stimulus. Little is known about the effects of androgens on inflammation in human vascular tissues. Therefore, we tested the hypothesis that DHT alters COX-2 levels in both the absence and presence of induced inflammation in primary human coronary artery smooth muscle cells (HCASMC). Furthermore, we tested the ancillary hypothesis that DHT's effects on COX-2 levels are AR-dependent. Cells were treated wi...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3215138</comments>
            <pubDate>Tue, 26 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3215138</guid>        </item>
        <item>
            <title>Inappropriate glucagon response after oral as compared to isoglycemic intravenous glucose administration in patients with type 1 diabetes.</title>
            <link>http://www.medworm.com/index.php?rid=3215137&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20103744%26dopt%3DAbstract</link>
            <description>Authors: Hare K, Vilsb&amp;#xF8;ll T, Holst JJ, Knop FK
    Hyperglucagonemia following oral glucose ingestion in patients with type 1 diabetes (and type 2 diabetes) has been claimed to result from impaired intra-islet insulin inhibition of glucagon. We looked at plasma glucagon responses to oral glucose tolerance test (OGTT) and isoglycemic intravenous (iv) glucose infusion (IIGI), respectively, in patients with type 1 diabetes. Nine patients without residual beta cell function (age: 25+/-9 years; body mass index (BMI): 24+/-2 kg/m(2); fasting plasma glucose (FPG): 9.5+/-2.1 mM; HbA1c: 8.4+/-1.2% (mean+/-standard deviation)) and 8 healthy subjects (age: 28+/-5 years; BMI: 24+/-3 kg/m(2); FPG: 5.3+/-0.2 mM; HbA1c: 5.0+/-0.1%) were examined on two separate occasions: 4-hour 50 g-OGTT and IIGI. ...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3215137</comments>
            <pubDate>Tue, 26 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3215137</guid>        </item>
        <item>
            <title>Chronic Exposure to Elevated Norepinephrine Suppresses Insulin Secretion in Fetal Sheep with Placental Insufficiency and Intrauterine Growth Restriction.</title>
            <link>http://www.medworm.com/index.php?rid=3198242&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20086198%26dopt%3DAbstract</link>
            <description>In this study, we examined chronic norepinephrine suppression of insulin secretion in sheep fetuses with placental insufficiency-induced intrauterine growth restriction (IUGR). Glucose stimulated insulin secretion (GSIS) was measured with a square-wave hyperglycemic clamp in the presence or absence of adrenergic receptor antagonists, phentolamine (alpha) and propranolol (beta). IUGR fetuses were hypoglycemic, hypoxemic, and had lower GSIS responsiveness (P&amp;lt;/=0.05) compared to control fetuses. IUGR fetuses also had elevated plasma norepinephrine (3264+/-614 vs. 570+/-86 pg/mL; P&amp;lt;/=0.05) and epinephrine (164+/-32 vs. 60+/-12 pg/mL; P&amp;lt;/=0.05) concentrations. In control fetuses, adrenergic inhibition increased baseline plasma insulin concentrations (1.7 fold, P&amp;lt;/=0.05), whereas dur...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3198242</comments>
            <pubDate>Tue, 19 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3198242</guid>        </item>
        <item>
            <title>The effect of dietary fat content on phospholipid fatty acid profile is muscle fiber-type dependent.</title>
            <link>http://www.medworm.com/index.php?rid=3198241&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20086199%26dopt%3DAbstract</link>
            <description>Authors: Janovska A, Hatzinikolas G, Mano M, Wittert GA
    A high saturated fat diet (HFD) induces obesity and insulin resistance (IR). IR has been linked to alterations and increased saturation in the phospholipid composition of skeletal muscles. We aimed to determine whether HFD feeding affects fatty acid (FA) membrane profile in a muscle fiber-type specific manner. We measured phospholipid FAs and expression of FA synthesis genes in oxidative soleus (SOL) and glycolytic extensor digitorum longus (EDL) muscles from rats fed either standard chow (SLD) or a HFD. The HFD increased fat mass, plasma insulin and leptin levels. Compared with EDL, SOL muscles preferentially accumulated C18 over C16 FAs and n-6 over n-3 polyunsaturated FAs (PUFAs) on either diet. With the HFD, SOL muscles contai...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3198241</comments>
            <pubDate>Tue, 19 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3198241</guid>        </item>
        <item>
            <title>The microRNA miR-696 regulates PGC1alpha in mouse skeletal muscle in response to physical activity.</title>
            <link>http://www.medworm.com/index.php?rid=3198240&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20086200%26dopt%3DAbstract</link>
            <description>Authors: Aoi W, Naito Y, Mizushima K, Takanami Y, Kawai Y, Ichikawa H, Yoshikawa T
    MicroRNAs (miRNAs) are small non-coding RNA involved in post-transcriptional gene regulation that have been shown to be involved in growth, development, function, and stress responses of various organs. The purpose of this study was to identify the miRNA response to physical activity, which was related to functions such as nutrient metabolism, although the miRNAs involved are currently unknown. C57BL/6 mice were divided into exercise and control groups. The exercise group performed running exercise with a gradual increase of the load over 4 weeks. On the other hand, to examine the effect of muscle inactivity, the unilateral hind limb of other mice was fixed in a cast for 5 days. Microarray analysis for m...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3198240</comments>
            <pubDate>Tue, 19 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3198240</guid>        </item>
        <item>
            <title>Exercise-training versus diet-induced weight-loss on metabolic risk factors and inflammatory markers in obese subjects.A 12-week randomized intervention-study.</title>
            <link>http://www.medworm.com/index.php?rid=3198239&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20086201%26dopt%3DAbstract</link>
            <description>In conclusion, rather large weight losses (more than 5-7%) were found to have beneficial effects on circulating inflammatory markers in these obese subjects. Aerobic exercise for 12weeks which increased VO2max was found to have no effects on circulating inflammatory markers in these obese patients. It is suggested that more intensive exercise may be necessary to affect systemic inflammation.
    PMID: 20086201 [PubMed - as supplied by publisher] (Source: Am J Physiol Endocri...)</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3198239</comments>
            <pubDate>Tue, 19 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3198239</guid>        </item>
        <item>
            <title>Progesterone inhibits glucose uptake by affecting diverse steps of insulin signaling in 3T3-L1 adipocytes.</title>
            <link>http://www.medworm.com/index.php?rid=3174262&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20071559%26dopt%3DAbstract</link>
            <description>Authors: Wada T, Hori S, Sugiyama M, Fujisawa E, Nakano T, Tsuneki H, Nagira K, Saito S, Sasaoka T
    Maternal insulin resistance is essential for efficient provision of glucose to the fetus. Although elevation of placental hormones is known to relate to the development of insulin resistance, the precise underlying mechanism of maternal insulin resistance is unknown. Therefore, we examined the molecular mechanisms of progesterone causing insulin resistance in 3T3-L1 adipocytes. Progesterone at 10(-4) M, but not 10(-5) M reduced the amount of IRS1. As a result, insulin-induced phosphorylation of IRS1, the association of IRS1 with p85alpha, and subsequent phosphorylation of Akt-1,-2 was moderately decreased by 10(-4) M progesterone. Subsequently, insulin-induced translocation of Glut4 to th...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3174262</comments>
            <pubDate>Wed, 13 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3174262</guid>        </item>
        <item>
            <title>Combining short-term metformin treatment and one bout of exercise does not increase insulin action in insulin resistant individuals.</title>
            <link>http://www.medworm.com/index.php?rid=3174261&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20071560%26dopt%3DAbstract</link>
            <description>Authors: Sharoff CG, Hagobian TA, Malin SK, Chipkin SR, Yu H, Hirshman MF, Goodyear LJ, Braun B
    The results from the Diabetes Prevention Program highlight the effectiveness of metformin and regular physical activity in the prevention of Type 2 diabetes. The mechanism by which these treatments prevent diabetes is by improving insulin sensitivity. Metformin and exercise independently increase insulin sensitivity; however, the combined effects have not been studied. To assess the combined effects, we studied 2 groups of insulin resistant subjects matched for, weight, body fat, fitness and degree of insulin resistance. The 1st group (n=9) was studied before treatment (B), after 2-3 weeks of 2000 mg/day metformin (MET), and after metformin plus 40min of exercise at 65%VO(2peak) (MET+Ex). Th...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3174261</comments>
            <pubDate>Wed, 13 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3174261</guid>        </item>
        <item>
            <title>Triacylglycerol lipases and metabolic control: implications for health and disease.</title>
            <link>http://www.medworm.com/index.php?rid=3174260&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20071561%26dopt%3DAbstract</link>
            <description>Authors: Watt MJ, Spriet LL
    Fatty acids derived from the hydrolysis of adipose tissue and skeletal muscle triacylglycerol (TG) are an important energy substrate at rest and during physical activity. This review outlines the identification of the new TG lipase, adipose triglyceride lipase, the current understanding of how cellular TG lipases are regulated, and the implications for understanding the integrated control of TG lipolysis. Further, this review outlines recent advances that propose a 'revised' role for TG lipases in cellular function, metabolic homeostasis and disease prevention.
    PMID: 20071561 [PubMed - as supplied by publisher] (Source: Am J Physiol Endocri...)</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3174260</comments>
            <pubDate>Wed, 13 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3174260</guid>        </item>
        <item>
            <title>Glucose-Dependent Blood Flow Dynamics in Murine Pancreatic Islets In Vivo.</title>
            <link>http://www.medworm.com/index.php?rid=3174259&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20071562%26dopt%3DAbstract</link>
            <description>Authors: Nyman LR, Ford E, Powers AC, Piston DW
    Pancreatic islets are highly vascularized and arranged so that regions containing beta-cells are distinct from those containing other cell types. While islet blood flow has been studied extensively, little is known about the dynamics of islet blood flow during hypoglycemia or hyperglycemia. To investigate changes in islet blood flow as a function of blood glucose level, we clamped blood glucose sequentially at hyperglycemic (~300 mg/dl or 16.8 mM) and hypoglycemic (~50 mg/dl or 2.8 mM) levels while simultaneously imaging intra-islet blood flow in mouse models that express GFP in the beta-cells or yellow fluorescent protein (YFP) in the alpha-cells. Using line-scanning, confocal microscopy, in vivo blood flow was assayed after intravenous ...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3174259</comments>
            <pubDate>Wed, 13 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3174259</guid>        </item>
        <item>
            <title>Activation of the cardiac mTOR/p70S6K pathway by leucine requires PDK1 and correlates with PRAS40 phosphorylation.</title>
            <link>http://www.medworm.com/index.php?rid=3149734&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20051528%26dopt%3DAbstract</link>
            <description>In this study, we investigated whether PDK1 could also participate in the events leading to mTOR/p70S6K activation in response to leucine in the heart. In wild-type hearts, both leucine and insulin increased p70S6K activity while, in contrast to insulin, leucine was unable to activate PKB/Akt. The changes in p70S6K activity induced by insulin and leucine correlated with changes in phosphorylation of Thr-389, the mTOR-phosphorylation site on p70S6K, and of Ser-2448 on mTOR, both related to mTOR activity. Leucine also triggered phosphorylation of the proline-rich Akt/PKB substrate of 40 kDa (PRAS40), a new pivotal mTOR regulator. In PDK1 knockout hearts, leucine, similarly to insulin, failed to induce the phosphorylation of mTOR and p70S6K, leading to the absence of p70S6K activation. The lo...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3149734</comments>
            <pubDate>Tue, 05 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3149734</guid>        </item>
        <item>
            <title>Orexin activation precedes increased npy expression, hyperphagia and metabolic changes in response to sleep deprivation.</title>
            <link>http://www.medworm.com/index.php?rid=3149733&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20051529%26dopt%3DAbstract</link>
            <description>In conclusion, orexin activation accounts for the myriad of changes induced by sleep deprivation, especially the hyperphagia induced under stress and a negative energy balance.
    PMID: 20051529 [PubMed - as supplied by publisher] (Source: Am J Physiol Endocri...)</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3149733</comments>
            <pubDate>Tue, 05 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3149733</guid>        </item>
        <item>
            <title>Unfolding the mechanisms of disease progression in permanent neonatal diabetes.</title>
            <link>http://www.medworm.com/index.php?rid=3149732&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20051530%26dopt%3DAbstract</link>
            <description>Authors: Dhanvantari S
    not applicable.
    PMID: 20051530 [PubMed - as supplied by publisher] (Source: Am J Physiol Endocri...)</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3149732</comments>
            <pubDate>Tue, 05 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3149732</guid>        </item>
        <item>
            <title>Metabolic interactions among dietary cholesterol, copper, and fructose.</title>
            <link>http://www.medworm.com/index.php?rid=3101328&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20009038%26dopt%3DAbstract</link>
            <description>Authors: Klevay LM
    
    PMID: 20009038 [PubMed - in process] (Source: Am J Physiol Endocri...)</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3101328</comments>
            <pubDate>Fri, 18 Dec 2009 18:58:05 +0100</pubDate>
            <guid isPermaLink="false">3101328</guid>        </item>
        <item>
            <title>PKA-dependent potentiation of glucose-stimulated insulin secretion by Epac activator 8-pCPT-2'-O-Me-cAMP-AM in human islets of Langerhans.</title>
            <link>http://www.medworm.com/index.php?rid=3101338&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20009023%26dopt%3DAbstract</link>
            <description>Authors: Chepurny OG, Kelley GG, Dzhura I, Leech CA, Roe MW, Dzhura E, Li X, Schwede F, Genieser HG, Holz GG
    Potential insulin secretagogue properties of an acetoxymethyl ester of a cAMP analog (8-pCPT-2'-O-Me-cAMP-AM) that activates the guanine nucleotide exchange factors Epac1 and Epac2 were assessed using isolated human islets of Langerhans. RT-QPCR demonstrated that the predominant variant of Epac expressed in human islets was Epac2, although Epac1 was detectable. Under conditions of islet perifusion, 8-pCPT-2'-O-Me-cAMP-AM (10 micromolar) potentiated first and second phase 10 mM glucose-stimulated insulin secretion (GSIS), while failing to influence insulin secretion measured in the presence of 3 mM glucose. The insulin secretagogue action of 8-pCPT-2'-O-Me-cAMP-AM was associated ...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3101338</comments>
            <pubDate>Tue, 15 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3101338</guid>        </item>
        <item>
            <title>Effects of fructosamine-3-kinase deficiency on function and survival of mouse pancreatic islets after prolonged culture in high glucose or ribose concentrations.</title>
            <link>http://www.medworm.com/index.php?rid=3101337&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20009024%26dopt%3DAbstract</link>
            <description>Authors: Pascal SM, Veiga-da-Cunha M, Gilon P, Van Schaftingen E, Jonas JC
    Due to their high glucose permeability, insulin secreting pancreatic beta-cells likely undergo strong intracellular protein glycation at high glucose concentrations. They may, however, be partly protected from the glucotoxic alterations of their survival and function by fructosamine-3-kinase (FN3K), a ubiquitous enzyme that initiates deglycation of intracellular proteins. To test that hypothesis, we cultured pancreatic islets from Fn3k knockout (Fn3k(-/-)) mice and their wild-type (WT) littermates for one to three weeks in the presence of 10 or 30 mmol/l glucose (G10-G30) and measured protein glycation, apoptosis, preproinsulin gene expression, and Ca(2+) and insulin secretory responses to acute glucose stimulat...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3101337</comments>
            <pubDate>Tue, 15 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3101337</guid>        </item>
        <item>
            <title>Cellular modeling: insight into oral minimal models of insulin secretion.</title>
            <link>http://www.medworm.com/index.php?rid=3101336&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20009025%26dopt%3DAbstract</link>
            <description>Authors: Pedersen MG, Toffolo GM, Cobelli C
    The oral glucose tolerance test (OGTT) and meal tolerance test are common clinical tests of the glucose-insulin system. Several mathematical models have been suggested as means to extract information about beta-cell function from data from oral tolerance tests. Any such model needs necessarily to be fairly simple but should at the same time be linked to the underlying biology of the insulin secreting beta-cells. The scope of the present work is to present a way to make such a connection using a recent model describing intracellular mechanisms. We show how the three main components of oral minimal secretion models, derivative control, proportional control and delay, are related to subcellular events, thus providing mechanistic underpinning of ...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3101336</comments>
            <pubDate>Tue, 15 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3101336</guid>        </item>
        <item>
            <title>Skeletal muscle glucose uptake during contraction is regulated by nitric oxide and ROS independently of AMPK.</title>
            <link>http://www.medworm.com/index.php?rid=3101335&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20009026%26dopt%3DAbstract</link>
            <description>In conclusion, ROS and NO are involved in regulating skeletal muscle glucose uptake during contraction via an AMPK-independent mechanism.
    PMID: 20009026 [PubMed - as supplied by publisher] (Source: Am J Physiol Endocri...)</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3101335</comments>
            <pubDate>Tue, 15 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3101335</guid>        </item>
        <item>
            <title>Lack of functional GABAB receptors alters GnRH physiology and sexual dimorphic expression of GnRH and GAD-67 in the brain.</title>
            <link>http://www.medworm.com/index.php?rid=3101334&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20009027%26dopt%3DAbstract</link>
            <description>Authors: Catalano PN, Di Giorgio NP, Bonaventura MM, Bettler B, Libertun C, Lux-Lantos VA
    GABA, the main inhibitory neurotransmitter, acts through GABA(A/C) and GABA(B) receptors (GABA(B)Rs); it is critical for gonadotropin regulation. We studied whether the lack of functional GABA(B)Rs in GABA(B1) knock-out mice (GABA(B1)KO) affected the gonadotropin axis physiology. Adult male and female GABA(B1)KO and wild-type (WT) mice were sacrificed to collect blood and tissue samples. Gonadotropin releasing hormone (GnRH) content in whole hypothalami (HT), olfactory bulbs (OB) and frontoparietal cortices (CT) were determined (RIA). GnRH expression by real-time PCR (qRT-PCR) was evaluated in preoptic area-anterior hypothalamus (POA-AH), medialbasal-posterior hypothalamus (MBH-PH), OB and CT. Pul...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3101334</comments>
            <pubDate>Tue, 15 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3101334</guid>        </item>
        <item>
            <title>RS4-Type Resistant Starch Prevents High-Fat Diet-Induced Obesity via Increased Hepatic Fatty Acid Oxidation and Decreased Postprandial GIP in C57BL/6J Mice.</title>
            <link>http://www.medworm.com/index.php?rid=3101333&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20009028%26dopt%3DAbstract</link>
            <description>In conclusion, dietary supplementation with RS4-type resistant starch attenuates high-fat diet-induced obesity more effectively than RS2 in C57BL/6J mice, which may be attributable to lower postprandial GIP and increased fat catabolism in the liver.
    PMID: 20009028 [PubMed - as supplied by publisher] (Source: Am J Physiol Endocri...)</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3101333</comments>
            <pubDate>Tue, 15 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3101333</guid>        </item>
        <item>
            <title>Characterization of Purinergic P2X4 Receptor Channels Expressed in Anterior Pituitary Cells.</title>
            <link>http://www.medworm.com/index.php?rid=3101332&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20009029%26dopt%3DAbstract</link>
            <description>Authors: Zemkova H, Kucka M, Li S, Gonzalez-Iglesias AE, Tomic M, Stojilkovic SS
    Anterior pituitary cells express cation conducting P2X receptor channels (P2XRs), but their molecular identity, electrophysiological properties, cell-specific expression pattern, and physiological roles have been only partially characterized. Here, we show by quantitative RT-PCR that mRNA transcripts for the P2X(4) subunit are the most abundant in rat anterior pituitary tissue and confirm the P2X(4)R protein expression by western blot analysis. Single-cell patch clamp recordings show that extracellular ATP induced an inward depolarizing current in a majority of thyrotropin-releasing hormone-responsive pituitary cells, which resembled the current profile generated by recombinant P2X(4)R. The channels were a...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3101332</comments>
            <pubDate>Tue, 15 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3101332</guid>        </item>
        <item>
            <title>Over-expression of Foxf2 in adipose tissue is associated with lower levels of IRS1 and decreased glucose uptake in vivo.</title>
            <link>http://www.medworm.com/index.php?rid=3101331&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20009030%26dopt%3DAbstract</link>
            <description>Authors: Westergren R, Nilsson D, Heglind M, Arani Z, Grande M, Cederberg A, Ahren B, Enerback S
    Many members of the forkhead genes family of transcription factors have been implicated as important regulators of metabolism, in particular glucose homeostasis e.g. Foxo1, Foxa3 and Foxc2. The purpose of this study was to exploit the possibility that yet unknown members of this gene family play a role in regulating glucose tolerance in adipocytes. We identified Foxf2 in a screen for adipose expressed forkhead genes. In vivo over-expression of Foxf2 in an adipose tissue restricted fashion demonstrated that such mice display a significantly induced insulin secretion in response to an intravenous glucose load as compared with wild type littermates. In response to increased Foxf2 expression, I...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3101331</comments>
            <pubDate>Tue, 15 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3101331</guid>        </item>
        <item>
            <title>Glucose transporters in the 21st Century.</title>
            <link>http://www.medworm.com/index.php?rid=3101330&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20009031%26dopt%3DAbstract</link>
            <description>Authors: Thorens B, Mueckler MM
    None.
    PMID: 20009031 [PubMed - as supplied by publisher] (Source: Am J Physiol Endocri...)</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3101330</comments>
            <pubDate>Tue, 15 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3101330</guid>        </item>
        <item>
            <title>Early Exposure of the Pregestational Intrauterine and Postnatal Growth Restricted Female Offspring to a Peroxisome Proliferator-Activated Receptor {gamma} Agonist.</title>
            <link>http://www.medworm.com/index.php?rid=3101329&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20009032%26dopt%3DAbstract</link>
            <description>Authors: Garg M, Thamotharan M, Pan G, Lee PW, Devaskar SU
    Prenatal nutrient restriction with intrauterine growth restriction (IUGR) alters basal and glucose stimulated insulin response and hepatic metabolic adaptation. The effect of early intervention with insulin sensitizing PPARgamma agonists was examined in the metabolically maladapted F1 pre-gestational IUGR offspring with a propensity towards pregnancy-induced gestational diabetes. The effect of rosiglitazone maleate (RG; 11 mumol/d from PN21 to PN60) versus placebo (PL) on metabolic adaptations in 2 m old F1 female rats subjected to prenatal (IUGR), postnatal (PNGR) or pre- and postnatal (IUGR+PNGR) nutrient restriction was investigated in comparison to control (CON). RG versus PL had no effect on body weight or plasma glucose c...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3101329</comments>
            <pubDate>Tue, 15 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3101329</guid>        </item>
        <item>
            <title>Injection of Urocortin 3 into the ventromedial hypothalamus modulates feeding, blood glucose levels and hypothalamic POMC gene expression but not the HPA axis.</title>
            <link>http://www.medworm.com/index.php?rid=3052888&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19952342%26dopt%3DAbstract</link>
            <description>In conclusion, the present study demonstrates that CRFR2 in the VMH mediates some of the central effects of Ucn 3 and the ARH melanocortin system may be a downstream target of VMH CRFR2 neurons.
    PMID: 19952342 [PubMed - as supplied by publisher] (Source: Am J Physiol Endocri...)</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3052888</comments>
            <pubDate>Tue, 01 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3052888</guid>        </item>
        <item>
            <title>In vitro processing and secretion of mutant insulin proteins that cause permanent neonatal diabetes.</title>
            <link>http://www.medworm.com/index.php?rid=3052887&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19952343%26dopt%3DAbstract</link>
            <description>Authors: Rajan S, Eames SC, Park SY, Labno C, Bell GI, Prince V, Philipson LH
    Permanent neonatal diabetes mellitus is a rare form of insulin-requiring diabetes presenting within the first few weeks or months of life. Mutations in the insulin gene are the second most common cause of this form of diabetes. These mutations are located in critical regions of preproinsulin and are likely to prevent normal processing or folding of the preproinsulin/proinsulin molecule. To characterize these mutations, we transiently expressed proinsulin-GFP fusion proteins in MIN6 mouse insulinoma cells. Our study revealed three groups of mutant proteins: (A) mutations that result in retention of proinsulin in the ER and attenuation of secretion of co-transfected wild-type insulin: C43G, F48C and C96Y; (B) m...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3052887</comments>
            <pubDate>Tue, 01 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3052887</guid>        </item>
        <item>
            <title>Nuclear receptors and hepatic lipidogenic enzymes response to a dyslipidemic sucrose rich diet and its revertion by fish oil n-3 polyunsaturated fatty acids.</title>
            <link>http://www.medworm.com/index.php?rid=3052886&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19952344%26dopt%3DAbstract</link>
            <description>In this study we examined the effect of SRD, after 8 months, on nuclear receptors, peroxisome-proliferator activated receptor-alpha (PPAR-alpha), and liver X receptor-alpha (LXR-alpha), stearoyl-CoA desaturase-1 (SCD-1), Delta6, and Delta5 desaturases mRNA and activity, hepatic enzymes involved in lipid metabolism, and fatty acid (FA) composition as well as the revertion produced by cod liver oil. SRD induced triglycerides increase in plasma and liver, increasing the anabolic FA synthase, malic enzyme and glucose 6-phosphate dehydrogenase, but not the pro-oxidative enzymes FA oxydase and carnitine palmitoyl transferase I, and correspondingly decreased PPAR-alpha and increased LXR-alpha expressions. Results suggest a contribution of both nuclear receptors interaction on these enzymatic acti...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3052886</comments>
            <pubDate>Tue, 01 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3052886</guid>        </item>
        <item>
            <title>Hexosamine biosynthesis pathway (HBP) flux promotes endoplasmic reticulum (ER) stress, lipid accumulation, and inflammatory gene expression in hepatic cells.</title>
            <link>http://www.medworm.com/index.php?rid=3052885&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19952345%26dopt%3DAbstract</link>
            <description>Authors: Sage AT, Walter LA, Shi Y, Khan MI, Kaneto H, Capretta F, Werstuck G
    There is increasing evidence that endoplasmic reticulum (ER) stress contributes to the development atherosclerosis in diabetes mellitus. The purpose of this study was to determine the effects of increased hexosamine biosynthesis pathway (HBP) flux on ER stress levels and the complications of ER stress associated with diabetes and atherosclerosis in hepatic cells. Glutamine:fructose-6-phosphate amidotransferase (GFAT), the rate limiting enzyme of the HBP, was overexpressed in HepG2 cells using an adenoviral expression system. The ER stress response and downstream effects, including activation of lipid and inflammatory pathways, were determined using real-time PCR, immunoblot analysis, and cell staining techniq...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3052885</comments>
            <pubDate>Tue, 01 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3052885</guid>        </item>
        <item>
            <title>Phenotypic and Pathomorphological Characteristics of a Novel Mutant Mouse Model for Maturity-Onset Diabetes of the Young Type 2 (MODY 2).</title>
            <link>http://www.medworm.com/index.php?rid=3052884&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19952346%26dopt%3DAbstract</link>
            <description>Authors: van Buerck L, Blutke A, Kautz S, Rathkolb B, Klaften M, Wagner S, Kemter E, Hrab&amp;#xE9; de Angelis M, Wolf E, Aigner B, W.e R, Herbach N
    Several mutant mouse models for human diseases such as diabetes mellitus have been generated in the large-scale Munich ENU (N-ethyl-N-nitrosourea) mouse mutagenesis project. The aim of this study was to identify the causal mutation of one of these strains and to characterize the resulting diabetic phenotype. Mutants exhibit a T to G transversion mutation at nt 629 in the glucokinase (Gck) gene, leading to an amino acid exchange from methionine to arginine at position 210. Adult Munich Gck(M210R) mutants demonstrated a significant reduction of hepatic glucokinase enzyme activity, but equal glucokinase mRNA and protein abundances. While homozygo...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3052884</comments>
            <pubDate>Tue, 01 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3052884</guid>        </item>
        <item>
            <title>Binge-pattern alcohol exposure during puberty induces sexually dimorphic changes in genes regulating the HPA axis.</title>
            <link>http://www.medworm.com/index.php?rid=3052883&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19952347%26dopt%3DAbstract</link>
            <description>In this study, we determined the effects of binge ethanol exposure during puberty on two critical central regulators of stress and anxiety behavior: corticotrophin-releasing hormone (CRH) and arginine vasopressin (AVP). Our results showed that ethanol increased plasma CORT levels in both sexes, yet binge-treated animals had significantly lower CORT levels than animals exposed to a single dose suggesting that the hypothalamo-pituitary-adrenal (HPA) axis habituated to the repeated stressful stimuli of ethanol. Binge ethanol exposure also significantly increased CRH and AVP gene expression in the PVN of males, but not females. Overall, our results demonstrate that binge ethanol exposure during puberty changes the central expression of stress related genes in a sex-specific manner, potentially...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3052883</comments>
            <pubDate>Tue, 01 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3052883</guid>        </item>
        <item>
            <title>High basal cell surface levels of fish GLUT4 are related to reduced sensitivity of insulin-induced translocation towards GGA and AS160 inhibition in adipocytes.</title>
            <link>http://www.medworm.com/index.php?rid=3052882&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19952348%26dopt%3DAbstract</link>
            <description>In this study we have characterized the intracellular and plasma membrane (PM) traffic of two orthologs of GLUT4 in fish, trout (btGLUT4) and salmon (okGLUT4), that do not share the amino terminal FQQI targeting motif of mammalian GLUT4. btGLUT4 (FQHL), and okGLUT4 (FQQL) to a lesser extent, showed higher basal PM levels, faster traffic to the PM after biosynthesis and earlier acquisition of insulin responsiveness than rat GLUT4. Furthermore, btGLUT4 showed a similar profile of internalization than rat GLUT4. Expression of the dominant-interfering AS160-4P mutant caused a significant decrease in the insulin-induced PM levels of okGLUT4 and rat GLUT4 and, to a lesser extent of btGLUT4, suggesting that btGLUT4 has reduced retention into the IRC. Contrary to rat GLUT4 and okGLUT4, the presenc...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3052882</comments>
            <pubDate>Tue, 01 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3052882</guid>        </item>
        <item>
            <title>Follicular origins of modern reproductive endocrinology.</title>
            <link>http://www.medworm.com/index.php?rid=3027367&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19933447%26dopt%3DAbstract</link>
            <description>Authors: Stephens SM, Moley KH
    This essay looks at the historical significance of the APS Classic Paper: Allen E, Doisy EA. The induction of a sexually mature condition in immature females by injection of the ovarian follicular hormone. Am J Physiol 69: 577-588, 1924 (http://ajplegacy.physiology.org/cgi/reprint/69/3/577).
    PMID: 19933447 [PubMed - in process] (Source: Am J Physiol Endocri...)</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3027367</comments>
            <pubDate>Thu, 26 Nov 2009 13:30:27 +0100</pubDate>
            <guid isPermaLink="false">3027367</guid>        </item>
        <item>
            <title>Portal Glucose Infusion-Glucose Clamp Measures Hepatic Influence on Postprandial Systemic Glucose Appearance as well as Whole-body Glucose Disposal.</title>
            <link>http://www.medworm.com/index.php?rid=3027366&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19934401%26dopt%3DAbstract</link>
            <description>Authors: Zheng D, Ionut V, Mooradian V, Stefanovski D, Bergman RN
    The full impact of the liver, through both glucose production and uptake, on systemic glucose appearance can not be readily studied in a classical glucose clamp because hepatic glucose metabolism is regulated not only by portal insulin and glucose levels but also portal glucose delivery (the portal signal). In the present study, we modified the classical glucose clamp by giving exogenous glucose through portal vein, the &quot;portal glucose infusion (PoG)-glucose clamp&quot;, to determine the net hepatic effect on postprandial systemic glucose supply along with the measurement of whole-body glucose disposal. By comparing systemic rate of glucose appearance (Ra) with portal glucose infusion (PoGinf), we quantified &quot;net hepatic gluc...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3027366</comments>
            <pubDate>Tue, 24 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3027366</guid>        </item>
        <item>
            <title>Pmch expression during early development is critical for normal energy homeostasis.</title>
            <link>http://www.medworm.com/index.php?rid=3027365&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19934402%26dopt%3DAbstract</link>
            <description>Authors: Mul J, Yi CX, van den Berg SA, Ruiter M, Toonen P, van der Elst M, Voshol PJ, Ellenbroek B, Kalsbeek A, la Fleur SE, Cuppen E
    Postnatal development and puberty are times of strong physical maturation and require large quantities of energy. The hypothalamic neuropeptide Melanin-Concentrating Hormone (MCH) regulates nutrient intake and energy homeostasis, but the underlying mechanisms are not completely understood. Here we use a novel rat knockout model in which the MCH-precursor Pmch has been inactivated to study the effects of loss of MCH on energy regulation in more detail. Pmch(-/-) rats are lean, hypophagic, osteoporotic, and although endocrine parameters were changed in pmch(-/-) rats, endocrine dynamics were normal, indicating an adaptation to new homeostatic levels rathe...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3027365</comments>
            <pubDate>Tue, 24 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3027365</guid>        </item>
        <item>
            <title>Impairment of fat oxidation under high vs low glycemic index diet occurs prior to the development of an obese phenotype.</title>
            <link>http://www.medworm.com/index.php?rid=3027364&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19934403%26dopt%3DAbstract</link>
            <description>Authors: Isken F, Klaus S, Petzke KJ, Loddenkemper C, Pfeiffer AF, Weickert MO
    Exposure to high vs low glycemic index (GI) diets increases fat mass and insulin resistance in obesity prone C57BL/6J mice. However, the longer-term effects and potentially involved mechanisms are largely unknown. We exposed four groups of male C57BL/6J mice (n = 10 per group) to long-term (20 weeks) or short-term (6 weeks) isoenergetic and macronutrient matched diets only differing in starch type and as such GI. Body composition, liver fat, molecular factors of lipid metabolism, and markers of insulin sensitivity and metabolic flexibility were investigated in all four groups of mice. Mice fed the high GI diet showed a rapid-onset (from week five) marked increase in body fat mass and liver fat, a gene expres...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3027364</comments>
            <pubDate>Tue, 24 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3027364</guid>        </item>
        <item>
            <title>Effect of a cyclooxygenase-2 inhibitor on postexercise muscle protein synthesis in humans.</title>
            <link>http://www.medworm.com/index.php?rid=3027363&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19934404%26dopt%3DAbstract</link>
            <description>Authors: Burd NA, Dickinson JM, Lemoine JK, Carroll CC, Sullivan BE, Haus JM, Jemiolo B, Trappe SW, Hughes GM, Sanders CE, Trappe TA
    Non-selective blockade of the cyclooxygenase (COX) enzymes in skeletal muscle eliminates the normal increase in muscle protein synthesis following resistance exercise. The current study tested the hypothesis that this COX-mediated increase in postexercise muscle protein synthesis is specifically regulated by the COX-2 isoform. Sixteen males (23+/-1y) were randomly assigned to one of two groups that received three doses of either a selective COX-2 inhibitor (celecoxib; 200 mg/dose, 600 mg total) or a placebo in double-blind fashion during the 24h following a single bout of knee extensor resistance exercise. At rest and 24h postexercise skeletal muscle prot...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3027363</comments>
            <pubDate>Tue, 24 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3027363</guid>        </item>
        <item>
            <title>A Kisspeptin-10 analogue with greater in vivo bioactivity than Kisspeptin-10.</title>
            <link>http://www.medworm.com/index.php?rid=3027362&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19934405%26dopt%3DAbstract</link>
            <description>Authors: Curtis AE, Cooke JH, Baxter JE, Parkinson JR, Bataveljic AS, Ghatei MA, Bloom SR, Murphy KG
    The kisspeptins are neuropeptides which stimulate the hypothalamo-pituitary-gonadal (HPG) axis. The smallest endogenous kisspeptin, kisspeptin-10 (KP-10), binds to the receptor KISS1R with a similar affinity to the full length peptide, kisspeptin-54 (KP-54), but is less effective in vivo, possibly due to increased enzymatic breakdown or clearance. The kisspeptin system may have therapeutic potential in the treatment of reproductive disorders and endocrine cancers. We have rationally modified the structure of KP-10 and tested the binding affinity of these analogues for the KISS1R. Those analogues which bound with relatively high affinity to KISS1R were tested for ability to stimulate ERK...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3027362</comments>
            <pubDate>Tue, 24 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3027362</guid>        </item>
        <item>
            <title>Protein Kinase C: Poised to Signal.</title>
            <link>http://www.medworm.com/index.php?rid=3027361&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19934406%26dopt%3DAbstract</link>
            <description>Authors: Newton A
    n/a.
    PMID: 19934406 [PubMed - as supplied by publisher] (Source: Am J Physiol Endocri...)</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3027361</comments>
            <pubDate>Tue, 24 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3027361</guid>        </item>
        <item>
            <title>Predicting Metabolic Adaptation, Body Weight Change and Energy Intake in Humans.</title>
            <link>http://www.medworm.com/index.php?rid=3027360&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19934407%26dopt%3DAbstract</link>
            <description>Authors: Hall KD
    Complex interactions between carbohydrate, fat, and protein metabolism underlie the body's remarkable ability to adapt to a variety of diets. But any imbalances between the intake and utilization rates of these macronutrients will result in changes of body weight and composition. Here, I present the first computational model that simulates how diet perturbations result in adaptations of fuel selection and energy expenditure that predict body weight and composition changes in both obese and non-obese men and women. No model parameters were adjusted to fit these data other than the initial conditions for each subject group (e.g., initial body weight and body fat mass). The model provides the first realistic simulations of how diet perturbations result in adaptations of w...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3027360</comments>
            <pubDate>Tue, 24 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3027360</guid>        </item>
        <item>
            <title>Calorie restriction increases fatty acid synthesis and whole body fat oxidation rates.</title>
            <link>http://www.medworm.com/index.php?rid=2970762&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19887594%26dopt%3DAbstract</link>
            <description>Authors: Bruss MD, Khambatta CF, Ruby MA, Aggarwal I, Hellerstein MK
    Calorie restriction (CR) increases longevity and retards the development of many chronic diseases, but the underlying metabolic signals are poorly understood. Increased fatty acid (FA) oxidation and reduced FA synthesis have been hypothesized to be important metabolic adaptations to CR. At metabolic steady state, however, FA oxidation must match FA intake plus synthesis; moreover, FA intake is low, not high, during CR. It is therefore not clear how FA dynamics are altered during CR. Accordingly, we measured food intake patterns, whole-body fuel selection, endogenous FA synthesis and gene expression in mice on CR. Within two days of starting CR, a shift occurred to a diurnal, cyclic pattern of whole-body FA metabolism,...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2970762</comments>
            <pubDate>Tue, 03 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2970762</guid>        </item>
        <item>
            <title>Skeletal Muscle NAMPT is Induced by Exercise in Humans.</title>
            <link>http://www.medworm.com/index.php?rid=2970761&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19887595%26dopt%3DAbstract</link>
            <description>Authors: Costford SR, Bajpeyi S, Pasarica M, Albarado DC, Thomas SC, Xie H, Church T, Jubrias SA, Conley KE, Smith SR
    In mammals, nicotinamide phosphoribosyltransferase (NAMPT) is responsible for the first and rate-limiting step in the conversion of nicotinamide to nicotinamide adenine dinucleotide (NAD(+)). NAD(+) is an obligate co-substrate for mammalian sirtuin 1 (SIRT1), a deacetylase which activates peroxisome proliferator-activated receptor gamma coactivator-1alpha (PGC-1alpha), which in turn can activate mitochondrial biogenesis. Given that mitochondrial biogenesis is activated by exercise, we hypothesized that exercise would increase NAMPT expression, as a potential mechanism leading to increased mitochondrial content in muscle. A cross-sectional analysis of human subjects show...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2970761</comments>
            <pubDate>Tue, 03 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2970761</guid>        </item>
        <item>
            <title>Potential role of autophagy in modulation of lipid metabolism.</title>
            <link>http://www.medworm.com/index.php?rid=2970760&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19887596%26dopt%3DAbstract</link>
            <description>Authors: Kovsan J, Bashan N, Greenberg A, Rudich A
    Autophagy is a major degradative pathway(s) by which intracellular components are delivered into the lysosomes. It is largely implicated in determining cell death and survival, because it eliminates un-necessary, damaged, and/or potentially harmful cellular products and organelles, and is an important source for nutrients and energy production under conditions of external nutrient deficiency. As such, autophagy has been suggested to contribute to the regulation of carbohydrate and protein metabolism during fasting. Recently, three papers implicated a role for autophagy in cellular lipid metabolism as well. This perspective article presents these novel findings in the context of prior studies on the role of autophagy and lysosomes in me...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2970760</comments>
            <pubDate>Tue, 03 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2970760</guid>        </item>
        <item>
            <title>AICAR and metformin, but not exercise, increase muscle glucose transport through AMPK- , ERK- and PDK1-dependent activation of atypical PKC.</title>
            <link>http://www.medworm.com/index.php?rid=2970759&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19887597%26dopt%3DAbstract</link>
            <description>Authors: Sajan MP, Bandyopadhyay G, Miura A, Standaert M, Nimal S, Longnus SL, Van Obberghen E, Hainault I, Foufelle F, Kahn CR, Braun U, Leitges M, Farese RV
    Activators of 5'-AMP-activated protein kinase (AMPK), 5-aminoimidazole-4-carboxamide-1-beta-4-ribofuranoside (AICAR), metformin and exercise activate atypical protein kinase C (aPKC) and ERK, and stimulate glucose transport in muscle by uncertain mechanisms. Here, in cultured L6-myotubes: AICAR- and metformin-induced activation of AMPK was required for activation of aPKC and ERK; aPKC activation involved and required phosphoinositide kinase-dependent-1 (PDK1) phosphorylation of thr-410-PKC-zeta; aPKC thr-410 phosphorylation and activation also required MEK1-dependent ERK; and glucose transport effects of AICAR and metformin were ...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2970759</comments>
            <pubDate>Tue, 03 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2970759</guid>        </item>
        <item>
            <title>Deficiency of Electron Transport Chain in Human Skeletal Muscle Mitochondria in Type 2 Diabetes Mellitus and Obesity.</title>
            <link>http://www.medworm.com/index.php?rid=2970758&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19887598%26dopt%3DAbstract</link>
            <description>Conclusions. The total activity of NADH-oxidase in biopsy for lean group is significantly higher than corresponding activity for obese or T2DM cohort. The specific activity of NADH-oxidase (per mg cardiolipin) and NADH-oxidase/citrate synthase and NADH-oxidase/beta-HAD ratios are reduced by 2-3 folds in both T2DM and obesity.
    PMID: 19887598 [PubMed - as supplied by publisher] (Source: Am J Physiol Endocri...)</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2970758</comments>
            <pubDate>Tue, 03 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2970758</guid>        </item>
        <item>
            <title>Peroxisome proliferator-activated receptor gamma (PPAR{gamma}) regulates the expression and Function of very low density lipoprotein receptor.</title>
            <link>http://www.medworm.com/index.php?rid=2939724&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19861583%26dopt%3DAbstract</link>
            <description>In this study, we have investigated the role of PPARgamma in the regulation of VLDLR expression and function in vivo and in vitro. During the differentiation of 3T3-L1 preadipocytes, the levels of VLDLR protein and mRNA increased in parallel to the induction of PPARgamma expression, and reached a maximum in mature adipocyte. Treatment of differentiated adipocytes with PPARgamma agonist pioglitazone upregulated VLDLR expression in dose- and time-dependent manners. In contrast, specific inhibition of PPARgamma significantly downregulated the protein level of VLDLR. Induction of VLDLR is also demonstrated in vivo in adipose tissue of wild type (WT) mice treated with pioglitazone. In addition, pioglitazone increased plasma TG-rich lipoprotein clearance and increased epididymal fat mass in WT m...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2939724</comments>
            <pubDate>Tue, 27 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2939724</guid>        </item>
        <item>
            <title>Interactions Between Neurotensin and GnRH Neurons in the Positive Feedback Control of GnRH/LH Secretion in the Mouse.</title>
            <link>http://www.medworm.com/index.php?rid=2939723&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19861584%26dopt%3DAbstract</link>
            <description>Authors: Dungan Lemko HM, Naderi R, Adjan V, Jennes L, Navarro VM, Clifton D, Steiner RA
    In female mammals, increased ovarian estradiol (E(2)) secretion triggers GnRH release from neurons in the basal forebrain, which drives LH secretion from the pituitary and subsequently induces ovulation; however, the neural circuits that activate this preovulatory GnRH/LH surge remain unidentified. Neurotensin is expressed in neurons of the anteroventral periventricular nucleus (AVPV), a region thought to be critical for generating the preovulatory GnRH/LH surge. E(2) induces neurotensin (Nts) gene expression in this region, and blockade of neurotensin signaling reduces the LH surge in the rat. We postulated that neurotensin signaling plays a similar role in generating the E(2)-induced GnRH/LH surg...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2939723</comments>
            <pubDate>Tue, 27 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2939723</guid>        </item>
        <item>
            <title>Apelin is necessary for the maintenance of insulin sensitivity.</title>
            <link>http://www.medworm.com/index.php?rid=2939722&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19861585%26dopt%3DAbstract</link>
            <description>CONCLUSIONS: Apelin is necessary for the maintenance of insulin sensitivity in vivo. Apelin's effects on glucose uptake and Akt phosphorylation are in part mediated by a Gi and AMPK-dependent pathway.
    PMID: 19861585 [PubMed - as supplied by publisher] (Source: Am J Physiol Endocri...)</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2939722</comments>
            <pubDate>Tue, 27 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2939722</guid>        </item>
        <item>
            <title>Endocrine pulse identification using penalized methods and a minimum set of assumptions.</title>
            <link>http://www.medworm.com/index.php?rid=2939721&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19861586%26dopt%3DAbstract</link>
            <description>Authors: Vis DJ, Westerhuis JA, Hoefsloot HC, Pijl H, Roelfsema F, van der Greef J, Smilde AK
    The detection of hormone secretion episodes is important for understanding normal and abnormal endocrine functioning, but pulse identification from hormones measured with short interval sampling is challenging. Furthermore, to obtain useable results, the model underlying hormone secretion and clearance must be augmented with restrictions based on biologically acceptable assumptions. Here, using the assumption that there are only a few time points at which a hormone is secreted, we used a modern penalized nonlinear least squares setup to select the number of secretion events. We did not assume a particular shape or frequency distribution for the secretion pulses. Our pulse identfication method,...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2939721</comments>
            <pubDate>Tue, 27 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2939721</guid>        </item>
        <item>
            <title>Constitutively active calcineurin in skeletal muscle increases endurance performance and mitochondrial respiratory capacity.</title>
            <link>http://www.medworm.com/index.php?rid=2939720&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19861587%26dopt%3DAbstract</link>
            <description>In conclusion our results provide evidence to support the hypothesis that calcineurin activation in skeletal muscle increases mitochondrial oxidative function and energy substrate storage, which contributes to enhanced endurance exercise performance. These adaptive changes occur as a consequence of a life-long expression of a constitutively active calcineurin and mimic the response to chronic endurance training.
    PMID: 19861587 [PubMed - as supplied by publisher] (Source: Am J Physiol Endocri...)</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2939720</comments>
            <pubDate>Tue, 27 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2939720</guid>        </item>
        <item>
            <title>The effect of different patterns of growth hormone administration on the IGF axis, somatic and skeletal growth of the dwarf rat.</title>
            <link>http://www.medworm.com/index.php?rid=2939719&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19861588%26dopt%3DAbstract</link>
            <description>This study demonstrates that aspects of growth are improved following introduction of infradian variation to GH treatment in a GH-deficient model. The data suggest that varying the pattern of GH doses administered to children may enhance growth performance without increasing the overall GH dose.
    PMID: 19861588 [PubMed - as supplied by publisher] (Source: Am J Physiol Endocri...)</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2939719</comments>
            <pubDate>Tue, 27 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2939719</guid>        </item>
        <item>
            <title>Am J Physiol Endocrinol Metab; +30 new citations</title>
            <link>http://www.medworm.com/index.php?rid=2852209&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fsites%2Fentrez%3Fcmd%3DSearch%26db%3Dpubmed%26term%3D%28%28%28Am%2520J%2520Physiol%2520Endocrinol%2520Metab%29%2520AND%2520%25222009%252F09%252F26%252005.30%2522%255BMHDA%255D%253A%25222009%252F10%252F01%252017.56%2522%255BMHDA%255D%29%29%2520NOT%2520%28%28%2520%28%28%28%2522Am%2520J%2520Physiol%2520Endocrinol%2520Metab%2522%255BTIAB%255D%29%29%29%2520AND%2520%25220001%2522%255BEDAT%255D%253A%25222009%252F09%252F26%252005.30%2522%255BEDAT%255D%29%29</link>
            <description>30 new pubmed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Physiol Endocrinol Metab
These pubmed results were generated on 2009/10/01PubMed, a service of the National Library of Medicine, includes over 15 million 
citations for biomedical articles back to the 1950's.
These citations are from MEDLINE and additional life science journals. 
PubMed includes links to many sites providing full text articles and other related resources. (Source: Am J Physiol Endocri...)</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2852209</comments>
            <pubDate>Thu, 01 Oct 2009 21:56:02 +0100</pubDate>
            <guid isPermaLink="false">2852209</guid>        </item>
        <item>
            <title>VLDL-TG kinetics: a dual isotope study for quantifying VLDL-TG pool size, production rates and fractional oxidation in humans.</title>
            <link>http://www.medworm.com/index.php?rid=2825291&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19773577%26dopt%3DAbstract</link>
            <description>Authors: Sorensen L, Gormsen L, Nielsen S
    Very-low-density-lipoproteins (VLDLs) are large, complex particles containing surface proteins (e.g. ApoB100) and core lipids (e.g. cholesterol and triglycerides). Whereas ApoB100 kinetics has been thoroughly studied, accurate measurement of VLDL-TG kinetics has proven difficult due to either complex mathematics or laborious procedures. The present study was therefore designed to measure VLDL-TG kinetics by dual isotope ex-vivo labeled VLDL-TG tracers and well established kinetics equations (bolus injection or the primed-continuous infusion). Ten healthy caucasian men (age 23+/-3 years (mean+/-SD), BMI 24.7+/-1.3kg/m(2)) were included in the study. VLDL-TG rate of appearance (Ra) was measured using a dual tracer technique ([9,10-(3)H]VLDL-TG an...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2825291</comments>
            <pubDate>Mon, 21 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2825291</guid>        </item>
        <item>
            <title>A Regulatory Role of LPCAT1 in the Synthesis of Inflammatory Lipids, PAF and LPC, in the Retina of Diabetic Mice.</title>
            <link>http://www.medworm.com/index.php?rid=2825290&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19773578%26dopt%3DAbstract</link>
            <description>Authors: Cheng L, Han X, Shi Y
    Platelet activation factor (PAF) and lysophosphotidylcholine (LPC) are potent inflammatory lipids. Elevated levels of PAF and LPC are associated with the onset of diabetic retinopathy and neurodegeneration. However, the molecular mechanisms underlying such defects remain elusive. LPCAT1 is a newly reported lysophospholipid acyltransferase implicated in anti-inflammatory response by converting LPC to PC. Intriguingly, the LPCAT1 enzyme also catalyzes the synthesis of PAF from lyso-PAF using acetyl-CoA as a substrate. The present studies investigated regulatory roles of LPCAT1 in the synthesis of inflammatory lipids during the onset of diabetes. Our work shows LPCAT1 plays an important role in the inactivation of PAF by catalyzing the synthesis of alkyl-PC,...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2825290</comments>
            <pubDate>Mon, 21 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2825290</guid>        </item>
        <item>
            <title>USP19 Deubiquitinating Enzyme Regulates Levels of Major Myofibrillar Proteins in L6 Muscle Cells.</title>
            <link>http://www.medworm.com/index.php?rid=2825289&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19773579%26dopt%3DAbstract</link>
            <description>Authors: Sundaram P, Pang Z, Miao M, Yu L, Wing S
    The ubiquitin-proteasome system plays an important role in the degradation of myofibrillar proteins that occurs in muscle wasting. Many studies have demonstrated the importance of enzymes mediating conjugation of ubiquitin. However, little is known about the role of deubiquitinating enzymes. We previously showed that the USP19 deubiquitinating enzyme is induced in atrophying skeletal muscle (Combaret et al. Amer. J. Physiol. 2005; 288: E693-E700). To further explore the role of USP19, we used siRNA in L6 muscle cells. Lowering USP19 by 70-90% in myotubes resulted in a 20% decrease in the rate of proteolysis and an 18% decrease in the rate of protein synthesis with no net change in protein content. Despite the decrease in overall synthes...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2825289</comments>
            <pubDate>Mon, 21 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2825289</guid>        </item>
        <item>
            <title>Effects of hormone-sensitive lipase-disruption on cardiac energy metabolism in response to fasting and refeeding.</title>
            <link>http://www.medworm.com/index.php?rid=2738471&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19706782%26dopt%3DAbstract</link>
            <description>Authors: Suzuki J, Ueno M, Uno M, Hirose Y, Zenimaru Y, Takahashi S, Osuga JI, Ishibashi S, Takahashi M, Hirose M, Yamada M, Kraemer FB, Miyamori I
    Increased fatty acid (FA) flux and intracellular lipid accumulation (steatosis) give rise to cardiac lipotoxicity in both pathological and physiological conditions. Since hormone-sensitive lipase (HSL) contributes to intracellular lipolysis in adipose tissue and heart, we investigated the impact of HSL-disruption on cardiac energy metabolism in response to fasting and refeeding. HSL-knockout (KO) mice and wildtype (Wt) littermates were fasted for 24 h followed by ~6 h of refeeding. Plasma FA concentration in Wt mice was elevated 2-fold with fasting, while KO mice lacked this elevation, resulting in 2-fold lower cardiac FA uptake compared to...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2738471</comments>
            <pubDate>Mon, 24 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2738471</guid>        </item>
        <item>
            <title>Editorial: The Search for the Membrane Thyroid Hormone Receptor.</title>
            <link>http://www.medworm.com/index.php?rid=2738470&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19706783%26dopt%3DAbstract</link>
            <description>Authors: Samson WK
    The 2009, Solomon Berson Award Lecture was delivered by Paul Davis, Director of the Ordway Research Institute in Albany, New York. In his invited review (5), which appears in this issue of the journal, Dr. Davis presents a compelling argument for the identity of the membrane thyroid hormone receptor, its signaling cascades and the physiologic importance of that hormone-receptor interaction.
    PMID: 19706783 [PubMed - as supplied by publisher] (Source: Am J Physiol Endocri...)</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2738470</comments>
            <pubDate>Mon, 24 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2738470</guid>        </item>
        <item>
            <title>Adipose Tissue Function and Dysfunction: Organ Cross-Talk and Metabolic Risk.</title>
            <link>http://www.medworm.com/index.php?rid=2738469&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19706784%26dopt%3DAbstract</link>
            <description>Authors: Giorgino F
    N/A. Key words: adipose tissue, visceral, cytokines, stem cells.
    PMID: 19706784 [PubMed - as supplied by publisher] (Source: Am J Physiol Endocri...)</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2738469</comments>
            <pubDate>Mon, 24 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2738469</guid>        </item>
        <item>
            <title>Comparison between Surrogate Indexes of Insulin Sensitivity/Resistance and Hyperinsulinemic Euglycemic Clamp Estimates in Rats.</title>
            <link>http://www.medworm.com/index.php?rid=2738468&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19706785%26dopt%3DAbstract</link>
            <description>Authors: Muniyappa R, Chen H, Muzumdar R, Einstein FH, Yan X, Yue LQ, Barzilai N, Quon MJ
    Assessing insulin resistance in rodent models gives insight into mechanisms that cause type 2 diabetes and the metabolic syndrome. The hyperinsulinemic euglycemic glucose clamp, the reference standard for measuring insulin sensitivity in humans and animals, is labor intensive and technically demanding. A number of simple surrogate indexes of insulin sensitivity/resistance have been developed and validated primarily for use in large human studies. These same surrogates are also frequently used in rodent studies. However, in general, these indexes have not been rigorously evaluated in animals. In a recent validation study in mice, we demonstrated that surrogates have a weaker correlation with glucos...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2738468</comments>
            <pubDate>Mon, 24 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2738468</guid>        </item>
        <item>
            <title>Acute glucose-lowering and insulin-sensitizing action of FGF21 in insulin resistant mouse models----Association with liver and adipose tissue effects.</title>
            <link>http://www.medworm.com/index.php?rid=2738467&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19706786%26dopt%3DAbstract</link>
            <description>Authors: Xu J, Stanislaus S, Chinookoswong N, Lau YY, Hager T, Patel J, Ge H, Weiszmann J, Lu SC, Graham M, Busby J, Hecht R, Li YS, Li Y, Lindberg RA, V&amp;#xE9;niant MM
    Recombinant FGF21 has anti-hyperglycemic, anti-hyperlipidemic, and anti-obesity effects in diabetic rodent and monkey models. Previous studies were confined to measuring steady state effects of FGF21 following subchronic or chronic administration. The current study focuses on the kinetics of biological actions of FGF21 following a single injection, and on the physiological and cellular mechanisms underlying FGF21 actions. We show that FGF21 resulted in rapid decline of blood glucose levels and immediate improvement of glucose tolerance and insulin sensitivity in two animal models of insulin resistance (i.e., ob/ob and DI...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2738467</comments>
            <pubDate>Mon, 24 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2738467</guid>        </item>
        <item>
            <title>Impact of type 1 diabetes on cardiac fibroblast activation: enhanced cell cycle progression and reduced myofibroblast content in the diabetic myocardium.</title>
            <link>http://www.medworm.com/index.php?rid=2738466&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19706787%26dopt%3DAbstract</link>
            <description>Authors: Shamhart PE, Luther DJ, Hodson BR, Koshy JC, Ohanyan V, Meszaros JG
    Diabetic patients are prone to developing myocardial fibrosis and suffer from decreased wound healing capabilities. The purpose of this study was to determine whether diabetes alters cardiac fibroblast activity in the myocardium in a 6 week streptozotocin-induced type 1 diabetic model. In vivo echocardiography indicated significant dilation of the left ventricle (LV) in the diabetic animals, while cardiac function was comparable to the normal group. We isolated cardiac fibroblasts from diabetic and control hearts and observed increased proliferation of the diabetic fibroblasts. Microarray analysis using mRNA collected from whole left ventricles revealed downregulation of known inhibitors of proliferation, p53 ...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2738466</comments>
            <pubDate>Mon, 24 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2738466</guid>        </item>
        <item>
            <title>Differential efficacy of sstr1, 2 and 5 agonists in the inhibition of c6 glioma growth in nude mice.</title>
            <link>http://www.medworm.com/index.php?rid=2738465&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19706788%26dopt%3DAbstract</link>
            <description>DIFFERENTIAL EFFICACY OF SSTR1, 2 AND 5 AGONISTS IN THE INHIBITION OF C6 GLIOMA GROWTH IN NUDE MICE.
    Am J Physiol Endocrinol Metab. 2009 Aug 25;
    Authors: Barbieri F, Pattarozzi A, Gatti M, Aiello C, Quintero A, Lunardi G, Bajetto A, Ferrari A, Culler MD, Florio T
    Somatostatin receptors (SSTR1-5) mediate antiproliferative effects. In C6 rat glioma cells, somatostatin is cytostatic in vitro via phosphotyrosine phosphatase-dependent inhibition of ERK1/2 activity, mediated by SSTR1, 2 and 5. Here we analyzed the effects of SSTR activation on C6 glioma growth in vivo and the intracellular mechanisms involved, comparing somatostatin effects with selective agonists for SSTR1, 2 and 5 (BIM-23745, BIM-23120, BIM-23206) or receptor bi-selective compounds (SSTR1+2, BIM-23704 and SSTR2+5, ...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2738465</comments>
            <pubDate>Mon, 24 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2738465</guid>        </item>
        <item>
            <title>TIP39/Parathyroid Hormone Type 2 Receptor Signaling is a Potent Inhibitor of Chondrocyte Proliferation and Differentiation.</title>
            <link>http://www.medworm.com/index.php?rid=2738464&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19706789%26dopt%3DAbstract</link>
            <description>Authors: Panda D, Goltzman D, Juppner H, Karaplis A
    Tuberoinfundibular peptide of 39 residues (TIP39) is a member of the parathyroid hormone (PTH) family of peptide hormones that exerts its function by interacting with the PTH type 2 receptor (PTH2R). Presently, no known function has been attributed to this signaling pathway in the developing skeleton. We observed that TIP39 and PTH2R were present in the newborn mouse growth plate with the receptor localizing in the resting zone whereas ligand expression was restricted exclusively in prehypertrophic and hypertrophic chondrocytes. By eight weeks of life PTH2R, and to a lesser degree TIP39, immunoreactivity was present in articular chondrocytes. We sought therefore to investigate the role of TIP39/PTH2R signaling in chondrocytes by gener...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2738464</comments>
            <pubDate>Mon, 24 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2738464</guid>        </item>
        <item>
            <title>Overexpression of the Nuclear Factor-{kappa}B subunit c-Rel protects against human islet cell death in vitro.</title>
            <link>http://www.medworm.com/index.php?rid=2738463&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19706790%26dopt%3DAbstract</link>
            <description>Authors: Mokhtari D, Barbu A, Mehmeti I, Vercamer C, Welsh N
    The transcription factor NF-kappaB is known to modulate rates of apoptosis and may therefore play a role in the increased beta-cell death that occurs in Type 1 and Type 2 diabetes. The aim of the present investigation was to study the expression of NF-kappaB subunits in human islet cells and whether over-expression of the NF-kappaB subunit c-Rel affects islet cell survival. We detected expression of p65, Rel-B, p50, p105, p52 and the ribosomal protein S3 (rpS3) in human islet cells. Among these, only p65 and rpS3 were translocated from the cytosolic to the nuclear fraction in response to cytokines. Interestingly, rpS3 participated in p65 binding to the kappaB-element in gel shift analysis experiments. We observed cytoplasmic ...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2738463</comments>
            <pubDate>Mon, 24 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2738463</guid>        </item>
        <item>
            <title>Novel liver-specific TORC2 siRNA corrects hyperglycemia in rodent models of type 2 diabetes.</title>
            <link>http://www.medworm.com/index.php?rid=2738462&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19706791%26dopt%3DAbstract</link>
            <description>In conclusion these results demonstrate the importance of TORC2 in modulating HGP in vivo, and highlight a novel, liver-specific siRNA approach for the potential treatment of hyperglycemia and type 2 diabetes. Key words: TORC2, siRNA, Diabetes.
    PMID: 19706791 [PubMed - as supplied by publisher] (Source: Am J Physiol Endocri...)</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2738462</comments>
            <pubDate>Mon, 24 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2738462</guid>        </item>
        <item>
            <title>Am J Physiol Endocrinol Metab; +40 new citations</title>
            <link>http://www.medworm.com/index.php?rid=2716629&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fsites%2Fentrez%3Fcmd%3DSearch%26db%3Dpubmed%26term%3D%28%28%28Am%2520J%2520Physiol%2520Endocrinol%2520Metab%29%2520AND%2520%25222009%252F08%252F14%252023.34%2522%255BMHDA%255D%253A%25222009%252F08%252F20%252011.46%2522%255BMHDA%255D%29%29%2520NOT%2520%28%28%2520%28%28%28%2522Am%2520J%2520Physiol%2520Endocrinol%2520Metab%2522%255BTIAB%255D%29%29%29%2520AND%2520%25220001%2522%255BEDAT%255D%253A%25222009%252F08%252F14%252023.34%2522%255BEDAT%255D%29%29</link>
            <description>40 new pubmed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Physiol Endocrinol Metab
These pubmed results were generated on 2009/08/20PubMed, a service of the National Library of Medicine, includes over 15 million 
citations for biomedical articles back to the 1950's.
These citations are from MEDLINE and additional life science journals. 
PubMed includes links to many sites providing full text articles and other related resources. (Source: Am J Physiol Endocri...)</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2716629</comments>
            <pubDate>Thu, 20 Aug 2009 15:46:02 +0100</pubDate>
            <guid isPermaLink="false">2716629</guid>        </item>
        <item>
            <title>Am J Physiol Endocrinol Metab; +30 new citations</title>
            <link>http://www.medworm.com/index.php?rid=2692777&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fsites%2Fentrez%3Fcmd%3DSearch%26db%3Dpubmed%26term%3D%28%28%28Am%2520J%2520Physiol%2520Endocrinol%2520Metab%29%2520AND%2520%25222009%252F08%252F07%252013.46%2522%255BMHDA%255D%253A%25222009%252F08%252F13%252002.36%2522%255BMHDA%255D%29%29%2520NOT%2520%28%28%2520%28%28%28%2522Am%2520J%2520Physiol%2520Endocrinol%2520Metab%2522%255BTIAB%255D%29%29%29%2520AND%2520%25220001%2522%255BEDAT%255D%253A%25222009%252F08%252F07%252013.46%2522%255BEDAT%255D%29%29</link>
            <description>30 new pubmed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Physiol Endocrinol Metab
These pubmed results were generated on 2009/08/13PubMed, a service of the National Library of Medicine, includes over 15 million 
citations for biomedical articles back to the 1950's.
These citations are from MEDLINE and additional life science journals. 
PubMed includes links to many sites providing full text articles and other related resources. (Source: Am J Physiol Endocri...)</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2692777</comments>
            <pubDate>Thu, 13 Aug 2009 06:36:01 +0100</pubDate>
            <guid isPermaLink="false">2692777</guid>        </item>
        <item>
            <title>Role of the atypical protein kinase Czeta in regulation of 5'-AMP-activated protein kinase in cardiac and skeletal muscle.</title>
            <link>http://www.medworm.com/index.php?rid=2638253&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19625676%26dopt%3DAbstract</link>
            <description>Authors: Ussher JR, Jaswal JS, Wagg CS, Armstrong HE, Lopaschuk DG, Keung W, Lopaschuk GD
    During metabolic stress, phosphorylation and activation of 5'-AMP-activated protein kinase (AMPK) becomes a major regulator of cellular energy metabolism in heart and skeletal muscle. Despite this, the upstream regulation of AMPK in both heart and muscle is poorly understood. Recent work has implicated the atypical protein kinase Czeta (PKCzeta) as a regulator of AMPK in endothelial cells via phosphorylation of LKB1, an upstream AMPK kinase (AMPKK). Our goal was to determine the potential role PKCzeta plays in regulating AMPK in cardiac and skeletal muscle. Cultures of H9c2 myocytes (cardiac) and C(2)C(12) myotubes (skeletal muscle) were pretreated with a selective PKCzeta pseudosubstrate peptide ...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2638253</comments>
            <pubDate>Sat, 25 Jul 2009 19:50:10 +0100</pubDate>
            <guid isPermaLink="false">2638253</guid>        </item>
        <item>
            <title>Leptin modulates ACAT1 expression and cholesterol efflux from human macrophages.</title>
            <link>http://www.medworm.com/index.php?rid=2638252&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19625677%26dopt%3DAbstract</link>
            <description>Authors: Hongo S, Watanabe T, Arita S, Kanome T, Kageyama H, Shioda S, Miyazaki A
    Leptin is an adipose tissue-derived hormone implicated in atherosclerosis and macrophage foam cell formation. The current study was conducted to examine the effect of leptin on cholesteryl ester accumulation in human monocytes/macrophages. Exogenously added leptin at 5 nM during differentiation of monocytes into macrophages for 7 days accelerated acetylated LDL (acetyl-LDL)-induced cholesteryl ester accumulation by 30-50%. Leptin did not affect endocytic uptake of acetyl-LDL; however, it increased ACAT activity 1.8-fold and ACAT-1 protein expression 1.9-fold. Among the four ACAT-1 mRNA transcripts, two shorter transcripts (2.8 and 3.6 kb) were upregulated approximately 1.7-fold upon leptin treatment. The ...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2638252</comments>
            <pubDate>Sat, 25 Jul 2009 19:50:07 +0100</pubDate>
            <guid isPermaLink="false">2638252</guid>        </item>
        <item>
            <title>Retraction.</title>
            <link>http://www.medworm.com/index.php?rid=2638251&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19625678%26dopt%3DAbstract</link>
            <description>Authors: 
    
    PMID: 19625678 [PubMed - in process] (Source: Am J Physiol Endocri...)</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2638251</comments>
            <pubDate>Sat, 25 Jul 2009 19:50:05 +0100</pubDate>
            <guid isPermaLink="false">2638251</guid>        </item>
        <item>
            <title>Enterostatin Deficiency Increases Serum Cholesterol but does not Influence Energy Homeostasis in Mice.</title>
            <link>http://www.medworm.com/index.php?rid=2631057&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19622781%26dopt%3DAbstract</link>
            <description>Authors: Miller R, D'Agostino D, Erlanson-Albertsson C, Lowe ME
    A pentapeptide released from procolipase, enterostatin, selectively attenuates dietary fat intake when administered peripherally or centrally. Enterostatin may act through the afferent vagus nerve and in the hypothalamus and amygdala, primarily in the central nucleus of the amygdala. To investigate the physiological role of endogenous enterostatin, we created an enterostatin-deficient, colipase-sufficient mouse (Ent(-/-)). Ent(-/-) mice are viable, normally active, and fertile. They exhibit normal growth on low-fat and high-fat diets. Furthermore, Ent(-/-) mice develop diet-induced obesity and have normal responses to a two-macronutrient choice diet and when switched from a high-fat diet to a low-fat diet. Ent(-/-) mice ha...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2631057</comments>
            <pubDate>Mon, 20 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2631057</guid>        </item>
        <item>
            <title>Selective Regulation of Cellular and Secreted Multimeric Adiponectin by Anti-Diabetic Therapies in Humans.</title>
            <link>http://www.medworm.com/index.php?rid=2631056&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19622782%26dopt%3DAbstract</link>
            <description>Authors: Phillips SA, Kung J, Ciaraldi TP, Choe C, Christiansen L, Mudaliar SR, Henry RR
    Adiponectin, an insulin-sensitizing factor secreted from adipose tissue, is decreased in individuals with type 2 diabetes (T2D) and increased in response to thiazolidinedione (TZD) therapy. Changes in its secretion and assembly into higher order forms affect insulin sensitivity. To determine the relative potency of TZDs on intra-adipocyte multimerization and secretion of adiponectin we assessed the impact of in vivo low- or high-dose rosiglitazone treatment alone or combined with metformin in subjects with T2D. T2D subjects received high-dose rosiglitazone (8 mg/day), high-dose metformin (2000 mg/day), or low-dose combination rosiglitazone/metformin therapy (4 mg+1000 mg/day) for 4 months. All subj...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2631056</comments>
            <pubDate>Mon, 20 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2631056</guid>        </item>
        <item>
            <title>Inflammation and impaired adipogenesis in hypertrophic obesity in man.</title>
            <link>http://www.medworm.com/index.php?rid=2631055&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19622783%26dopt%3DAbstract</link>
            <description>Authors: Gustafson B, Gogg S, Hedjazifar S, Jenndahl L, Hammarstedt A, Smith U
    Obesity is mainly associated with adipose cell enlargement in adult man (hypertrophic obesity) while the formation of new fat cells (hyperplastic obesity) predominates in the prepubertal age. Adipose cell size, independent of BMI, is negatively correlated with whole-body insulin sensitivity. We here review recent findings linking hypertrophic obesity with inflammation and a dysregulated adipose tissue including local cellular insulin resistance with reduced IRS-1 and GLUT-4 protein content. In addition, the number of preadipocytes in the abdominal subcutaneous adipose tissue capable of undergoing differentiation to adipose cells is reduced in hypertrophic obesity. This is likely to promote ectopic lipid accu...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2631055</comments>
            <pubDate>Mon, 20 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2631055</guid>        </item>
        <item>
            <title>Magnitude and control of mitochondrial adp sensitivity.</title>
            <link>http://www.medworm.com/index.php?rid=2631054&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19622784%26dopt%3DAbstract</link>
            <description>MAGNITUDE AND CONTROL OF MITOCHONDRIAL ADP SENSITIVITY.
    Am J Physiol Endocrinol Metab. 2009 Jul 21;
    Authors: Jeneson JA, Schmitz JP, van den Broek NM, van Riel NA, Hilbers P, Nicolay K, Prompers JJ
    The transduction function for ADP stimulation of mitochondrial ATP synthesis in skeletal muscle was reconstructed in vivo and in silico to investigate the magnitude and origin of mitochondrial sensitivity to cytoplasmic ADP concentration changes. Dynamic in vivo measurements of human leg muscle phosphocreatine (PCr) content during metabolic recovery from contractions were performed by (31)P NMR spectroscopy. The cytoplasmic ADP concentration ([ADP]) and rate of oxidative ATP synthesis (Jp) at each time point were calculated from creatine kinase equilibrium and the derivative of a mon...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2631054</comments>
            <pubDate>Mon, 20 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2631054</guid>        </item>
        <item>
            <title>TERTIARY ACTIVE TRANSPORT OF AMINO ACIDS RECONSTITUTED BY CO-EXPRESSION OF SYSTEM A AND L TRANSPORTERS IN Xenopus OOCYTES.</title>
            <link>http://www.medworm.com/index.php?rid=2631053&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19622785%26dopt%3DAbstract</link>
            <description>Authors: Baird F, Bett K, Maclean C, Tee AR, Hundal HS, Taylor PM
    The System L transporter facilitates cellular import of large neutral amino acids (AAs) such as Leu, a potent activator of the intracellular TOR pathway which signals for cell growth. System L is an AA exchanger, proposed to accumulate certain AAs by coupling to dissipation of concentration gradient(s) of exchange substrates generated by secondary active AA transporters such as System A. We addressed the hypothesis that this type of coupling (termed tertiary active transport) acts as an indirect mechanism to extend the range of AA stimulating TOR to those transported by both Systems A and L (e.g. glutamine) through downstream enhancement of leucine accumulation. System A (SNAT2) overexpression enabled Xenopus oocytes to ...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2631053</comments>
            <pubDate>Mon, 20 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2631053</guid>        </item>
        <item>
            <title>Characterization of contraction-inducible CXC chemokines and their roles in C2C12 myocytes.</title>
            <link>http://www.medworm.com/index.php?rid=2631052&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19622786%26dopt%3DAbstract</link>
            <description>Authors: Nedachi T, Hatakeyama H, Kono T, Sato M, Kanzaki M
    Physical exercise triggers the release of several cytokines/chemokines from working skeletal muscles, but the underlying mechanism(s) by which skeletal muscles decipher and respond to highly complex contractile stimuli remains largely unknown. In an effort to investigate the regulatory mechanisms of the expressions of two contraction-inducible CXC chemokines, CXCL1/KC and CXCL5/LIX, in contracting skeletal muscle cells, we took advantage of our in vitro exercise model using highly developed contractile C2C12 myotubes which acquire properties similar to those of in vivo skeletal muscle via manipulation of Ca(2+) transients with electric pulse stimulation (EPS). Production of these CXC chemokines was immediately augmented by EPS...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2631052</comments>
            <pubDate>Mon, 20 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2631052</guid>        </item>
        <item>
            <title>The effects of amino acids on glucose metabolism of isolated rat skeletal muscle are independent of insulin and the mTOR/S6k pathway.</title>
            <link>http://www.medworm.com/index.php?rid=2631051&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19622787%26dopt%3DAbstract</link>
            <description>Authors: Stadlbauer K, Brunmair B, Sz&amp;#xF6;cs Z, Krebs M, Luger A, F&amp;#xFC;rnsinn C
    Two mechanisms have been proposed for the modulation of skeletal muscle glucose metabolism by amino acids. Whereas studies on humans and cultured cells suggested acute insulin desensitization via mammalian target of rapamycin (mTOR) and its downstream target p70S6 kinase (S6k), investigations using native specimens of rat muscle hinted at impairment of glucose oxidation by competition for mitochondrial oxidation. To better understand these seemingly contradictory findings, we explored the effects of high concentrations of mixed amino acids on fuel metabolism and S6k activity in freshly isolated specimens of rat skeletal muscle. In this setting, increasing concentrations of amino acids dose-dependently re...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2631051</comments>
            <pubDate>Mon, 20 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2631051</guid>        </item>
        <item>
            <title>ERp46 is reduced by high glucose and regulates insulin content in pancreatic beta cells.</title>
            <link>http://www.medworm.com/index.php?rid=2631050&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19622788%26dopt%3DAbstract</link>
            <description>Conclusion. ERp46 may be an important component in the phenomenon of &quot;glucose toxicity&quot;, involved in insulin production at the post-translational level. Key words: pancreatic beta cells, glucose toxicity, proteomics, ERp46, insulin.
    PMID: 19622788 [PubMed - as supplied by publisher] (Source: Am J Physiol Endocri...)</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2631050</comments>
            <pubDate>Mon, 20 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2631050</guid>        </item>
        <item>
            <title>Am J Physiol Endocrinol Metab; +30 new citations</title>
            <link>http://www.medworm.com/index.php?rid=2612148&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fsites%2Fentrez%3Fcmd%3DSearch%26db%3Dpubmed%26term%3D%28%28%28Am%2520J%2520Physiol%2520Endocrinol%2520Metab%29%2520AND%2520%25222009%252F07%252F16%252010.18%2522%255BMHDA%255D%253A%25222009%252F07%252F18%252006.38%2522%255BMHDA%255D%29%29%2520NOT%2520%28%28%2520%28%28%28%2522Am%2520J%2520Physiol%2520Endocrinol%2520Metab%2522%255BTIAB%255D%29%29%29%2520AND%2520%25220001%2522%255BEDAT%255D%253A%25222009%252F07%252F16%252010.18%2522%255BEDAT%255D%29%29</link>
            <description>30 new pubmed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Physiol Endocrinol Metab
These pubmed results were generated on 2009/07/18PubMed, a service of the National Library of Medicine, includes over 15 million 
citations for biomedical articles back to the 1950's.
These citations are from MEDLINE and additional life science journals. 
PubMed includes links to many sites providing full text articles and other related resources. (Source: Am J Physiol Endocri...)</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2612148</comments>
            <pubDate>Sat, 18 Jul 2009 10:38:02 +0100</pubDate>
            <guid isPermaLink="false">2612148</guid>        </item>
        <item>
            <title>Am J Physiol Endocrinol Metab; +34 new citations</title>
            <link>http://www.medworm.com/index.php?rid=2606401&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fsites%2Fentrez%3Fcmd%3DSearch%26db%3Dpubmed%26term%3D%28%28%28Am%2520J%2520Physiol%2520Endocrinol%2520Metab%29%2520AND%2520%25222009%252F07%252F10%252021.30%2522%255BMHDA%255D%253A%25222009%252F07%252F16%252010.18%2522%255BMHDA%255D%29%29%2520NOT%2520%28%28%2520%28%28%28%2522Am%2520J%2520Physiol%2520Endocrinol%2520Metab%2522%255BTIAB%255D%29%29%29%2520AND%2520%25220001%2522%255BEDAT%255D%253A%25222009%252F07%252F10%252021.30%2522%255BEDAT%255D%29%29</link>
            <description>34 new pubmed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Physiol Endocrinol Metab
These pubmed results were generated on 2009/07/16PubMed, a service of the National Library of Medicine, includes over 15 million 
citations for biomedical articles back to the 1950's.
These citations are from MEDLINE and additional life science journals. 
PubMed includes links to many sites providing full text articles and other related resources. (Source: Am J Physiol Endocri...)</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2606401</comments>
            <pubDate>Thu, 16 Jul 2009 14:18:02 +0100</pubDate>
            <guid isPermaLink="false">2606401</guid>        </item>
        <item>
            <title>Am J Physiol Endocrinol Metab; +143 new citations</title>
            <link>http://www.medworm.com/index.php?rid=2533175&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fsites%2Fentrez%3Fcmd%3DSearch%26db%3Dpubmed%26term%3D%28%28%28Am%2520J%2520Physiol%2520Endocrinol%2520Metab%29%2520AND%2520%25222009%252F04%252F07%252017.31%2522%255BMHDA%255D%253A%25222009%252F06%252F27%252012.42%2522%255BMHDA%255D%29%29%2520NOT%2520%28%28%2520%28%28%28%2522Am%2520J%2520Physiol%2520Endocrinol%2520Metab%2522%255BTIAB%255D%29%29%29%2520AND%2520%25220001%2522%255BEDAT%255D%253A%25222009%252F04%252F07%252017.31%2522%255BEDAT%255D%29%29</link>
            <description>143 new pubmed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Physiol Endocrinol Metab
These pubmed results were generated on 2009/06/27PubMed, a service of the National Library of Medicine, includes over 15 million 
citations for biomedical articles back to the 1950's.
These citations are from MEDLINE and additional life science journals. 
PubMed includes links to many sites providing full text articles and other related resources. (Source: Am J Physiol Endocri...)</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2533175</comments>
            <pubDate>Sat, 27 Jun 2009 16:42:02 +0100</pubDate>
            <guid isPermaLink="false">2533175</guid>        </item>
        <item>
            <title>Biochemistry, Physiology, and Genetics of GPAT, AGPAT, and Lipin Enzymes in Triglyceride Synthesis.</title>
            <link>http://www.medworm.com/index.php?rid=2308644&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19336658%26dopt%3DAbstract</link>
            <description>Authors: Takeuchi K, Reue K
    Triacylglycerol (TAG) synthesis and storage in tissues such as adipose tissue and liver have an important role in metabolic homeostasis. The molecular identification of genes encoding enzymes that catalyze steps in TAG biosynthesis from glycerol-3-phosphate has revealed an unexpected number of protein isoforms of the glycerol phosphate acyltransferase (GPAT), acylglycerolphosphate acyltransferase (AGPAT), and lipin (phosphatidate phosphatase) families that appear to catalyze similar biochemical reactions. However, based on available data for a few members in which genetic deficiencies in mouse and/or human have been studied, we postulate that each GPAT, AGPAT, and lipin family member likely has a specialized role that may be uncovered through careful biochem...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2308644</comments>
            <pubDate>Tue, 31 Mar 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2308644</guid>        </item>
        <item>
            <title>Oral bovine lactoferrin improves bone status of ovariectomized mice.</title>
            <link>http://www.medworm.com/index.php?rid=2308643&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19336659%26dopt%3DAbstract</link>
            <description>In conclusion, these findings suggest that dietary lactoferrin supplementation have a beneficial effect on postmenopausal bone loss by modulating bone formation and resorption. Key words: Lactoferrin, Osteoblast, Osteoclast, bone.
    PMID: 19336659 [PubMed - as supplied by publisher] (Source: Am J Physiol Endocri...)</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2308643</comments>
            <pubDate>Tue, 31 Mar 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2308643</guid>        </item>
        <item>
            <title>Muscle inflammatory response and insulin resistance: synergistic interaction between macrophages and fatty acids leads to impaired insulin action.</title>
            <link>http://www.medworm.com/index.php?rid=2308642&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19336660%26dopt%3DAbstract</link>
            <description>In this study, we quantified macrophages immunohistochemically in vastus lateralis biopsies from 8 obese and 8 lean subjects. Our study demonstrates that macrophages infiltrate skeletal muscle in obesity and we developed an in vitro system to study this mechanistically. Myoblasts were isolated from vastus lateral biopsies and differentiated in culture. Co-culture of differentiated human myotubes with macrophages in the presence of palmitic acid, to mimic an obese environment, revealed that macrophages in the presence of palmitic acid synergistically augment cytokine and chemokine expression in myotubes, decrease IkappaBalpha protein expression, increase phosphorylated JNK, decrease phosphorylated AKT and increase markers of muscle atrophy. These results suggest that macrophages alter the i...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2308642</comments>
            <pubDate>Tue, 31 Mar 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2308642</guid>        </item>
        <item>
            <title>Iodide deficiency-induced angiogenic stimulus in the thyroid occurs via HIF- and reactive oxygen species (ROS)-dependent VEGF-A secretion from thyrocytes.</title>
            <link>http://www.medworm.com/index.php?rid=2308641&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19336661%26dopt%3DAbstract</link>
            <description>Authors: Gerard AC, Poncin S, Audinot JN, Denef JF, Colin I
    Vascular supply is an obvious requirement for all organs. In addition to oxygen and nutrients, blood flow also transports essential trace elements. Iodine, which is a key element in thyroid hormone synthesis, is one of them. An inverse relationship exists between the expansion of the thyroid microvasculature and the local availability of iodine. This microvascular trace element-dependent regulation is unique and contributes to keep steady the iodide delivery to the thyroid. Signals involved in this regulation, such as VEGF-A, originate from thyrocytes as early TSH-independent responses to iodide scarcity. The question raised in this paper is how thyrocytes, facing an acute drop in intracellular stores of iodine; generate angio...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2308641</comments>
            <pubDate>Tue, 31 Mar 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2308641</guid>        </item>
        <item>
            <title>Endothelial-specific tetrahydrobiopterin expression accelerates refractory wound healing by suppressing oxidative stress in diabetes.</title>
            <link>http://www.medworm.com/index.php?rid=2308639&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19336662%26dopt%3DAbstract</link>
            <description>Authors: Tie L, Li XJ, Wang X, Channon KM, Chen AF
    Refractory wound is a severe complication that leads to limb amputation in diabetes. Endothelial nitric oxide synthase (eNOS) plays a key role in normal wound repair, but is uncoupled in streptozotocin (STZ)-induced type 1 diabetes due to reduced cofactor tetrahydrobiopterin (BH4). We tested the hypothesis that overexpression of GTP cyclohydrolase I (GTPCH I), the rate-limiting enzyme for de novo BH4 synthesis, retards NOS uncoupling and accelerates wound healing in STZ mice. Blood glucose levels were significantly increased in both male endothelial-specific GTPCH I transgenic mice (Tg-GCH via a tie-2 promoter) and the wild-type (WT) littermates 5 days after STZ regimen. A full-thickness excisional wound was created on mouse dorsal ski...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2308639</comments>
            <pubDate>Tue, 31 Mar 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2308639</guid>        </item>
        <item>
            <title>Sulfur Amino Acid Deficiency Upregulates Intestinal Methionine Cycle Activity and Suppresses Epithelial Growth in Neonatal Pigs.</title>
            <link>http://www.medworm.com/index.php?rid=2277150&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19293331%26dopt%3DAbstract</link>
            <description>Authors: Bauchart-Thevret C, Stoll B, Chacko SK, Burrin DG
    We recently showed that the developing gut is a significant site of methionine (Met) transmethylation to homocysteine and transsulfuration to cysteine (Cys). We hypothesized that sulfur amino acid (SAA) deficiency would preferentially reduce mucosal growth and antioxidant function in neonatal piglets. Neonatal pigs were enterally-fed a control diet or SAA-free diet for 7 d and then whole-body methionine and cysteine kinetics were measured using an intravenous infusion of [1-(13)C;methyl-(2)H3]-Met and (15)N-Cys. Body weight gain and plasma Met, Cys, homocysteine, taurine and total erythrocyte glutathione concentrations were markedly decreased (-46 to -85%) in SAA-free vs. control pigs. Whole-body Met and Cys fluxes were reduced...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2277150</comments>
            <pubDate>Tue, 17 Mar 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2277150</guid>        </item>
        <item>
            <title>Association of Luteinizing Hormone Receptor Gene Expression with Cell Cycle Progression in Granulosa Cells.</title>
            <link>http://www.medworm.com/index.php?rid=2277148&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19293332%26dopt%3DAbstract</link>
            <description>Authors: Cannon JD, Seekallu S, Vandevoort CA, Chaffin CL
    During hormonally-induced ovarian follicle growth, granulosa cell proliferation increases and returns to baseline prior to the administration of an ovulatory stimulus. Several key genes appear to follow a similar pattern, including the luteinizing hormone receptor (LHCGR), suggesting an association between cell cycle progression and gene expression. The expression of LHCGR mRNA in granulosa cells isolated from immature rats and treated in culture with FSH increased in a time-dependent manner, while administration of the cell cycle inhibitor mimosine completely suppressed expression. While forskolin was able to induce luteinization in cells treated with mimosine, hCG had no effect, indicating the functional loss of LHCGR. The eff...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2277148</comments>
            <pubDate>Tue, 17 Mar 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2277148</guid>        </item>
        <item>
            <title>Transgenic mutant D567G but not wildtype human FSH receptor overexpression provides FSH-independent and promiscuous glycoprotein hormone Sertoli cell signaling.</title>
            <link>http://www.medworm.com/index.php?rid=2277146&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19293333%26dopt%3DAbstract</link>
            <description>Authors: Allan CM, Lim P, Robson M, Spaliviero J, Handelsman DJ
    We have characterized the in vivo actions of human wildtype FSH receptor overexpressed in Sertoli cells of transgenic mice (TgFSHRwt) compared transgenic overexpression of the human activated mutant FSHR*D567G (TgFSHR*D567G). Testicular TgFSHRwt expression significantly elevated specific FSH binding (&amp;gt;2-fold, P &amp;lt; 0.01) relative to non-transgenic testes, similar to increased FSH binding in TgFSHR*D567G testes. Isolated TgFSHRwt Sertoli cells exhibited higher FSH-stimulated cAMP levels compared to non-Tg or TgFSHR*D567G cells, but did not display the elevated FSH-independent basal cAMP levels found in TgFSHR*D567G Sertoli cells. Furthermore, Sertoli cell overexpression of TgFSHR*D567G but not TgFSHRwt allowed promiscuo...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2277146</comments>
            <pubDate>Tue, 17 Mar 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2277146</guid>        </item>
        <item>
            <title>Role for malic enzyme, pyruvate carboxylation and mitochondrial malate import in the glucose-stimulated insulin secretion.</title>
            <link>http://www.medworm.com/index.php?rid=2277144&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19293334%26dopt%3DAbstract</link>
            <description>In this report, we demonstrate that while adenoviral-mediated over-expression of ME1 greatly augments GSIS in rat insulinoma INS-1 832/13 cells, it does not restore MSSIS or significantly affect GSIS in mouse islets. The increase in GSIS following ME1 over-expression in INS-1 832/13 cells did not alter the ATP/ADP ratio, but was accompanied by increases in malate and citrate levels. Increased malate and citrate levels were also observed after providing INS-1 832/13 cells with the malate permeable analog dimethyl-malate (DMM). These data suggest that while ME1 over-expression augments anaplerosis and GSIS in INS-1 832/13 cells, it is not likely involved in MSSIS and GSIS in pancreatic islets. Key words: insulin secretion, pyruvate carboxylation, malic enzyme, dimethyl-malate.
    PMID: 1929...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2277144</comments>
            <pubDate>Tue, 17 Mar 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2277144</guid>        </item>
        <item>
            <title>Ligand-based gene expression profiling reveals novel roles of glucocorticoid receptor in cardiac metabolism.</title>
            <link>http://www.medworm.com/index.php?rid=2277141&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19293335%26dopt%3DAbstract</link>
            <description>Authors: Yoshikawa N, Nagasaki M, Sano M, Tokudome S, Ueno K, Shimizu N, Imoto S, Miyano S, Suematsu M, Fukuda K, Morimoto C, Tanaka H
    Recent studies have documented various roles of adrenal corticosteroid signaling in cardiac physiology and pathophysiology. It is known that glucocorticoids and aldosterone are able to bind glucocorticoid receptor (GR) and mineralocorticoid receptor (MR), and these ligand-receptor interactions are redundant. It, therefore, has been impossible to delineate how these nuclear receptors couple with corticosteroid ligands and differentially regulate gene expression for operation of their distinct functions in the heart. Here, to particularly define the role of GR in cardiac muscle cells, we applied ligand-based approach involving GR-specific agonist cortivaz...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2277141</comments>
            <pubDate>Tue, 17 Mar 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2277141</guid>        </item>
        <item>
            <title>Regulated Renin Release from 3T3-L1 Adipocytes.</title>
            <link>http://www.medworm.com/index.php?rid=2277139&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19293336%26dopt%3DAbstract</link>
            <description>In conclusion, the expression and secretion of renin are regulated under a complex series of hormonal and metabolic determinants in mature 3T3-L1 adipocytes. Key words: Adipocytes, Secretion, TNFalpha, Forskolin.
    PMID: 19293336 [PubMed - as supplied by publisher] (Source: Am J Physiol Endocri...)</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2277139</comments>
            <pubDate>Tue, 17 Mar 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2277139</guid>        </item>
        <item>
            <title>Diabetes induces and calcium channel blockers prevent cardiac expression of pro-apoptotic thioredoxin-interacting protein.</title>
            <link>http://www.medworm.com/index.php?rid=2238690&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19258488%26dopt%3DAbstract</link>
            <description>DIABETES INDUCES AND CALCIUM CHANNEL BLOCKERS PREVENT CARDIAC EXPRESSION OF PRO-APOPTOTIC THIOREDOXIN-INTERACTING PROTEIN.
    Am J Physiol Endocrinol Metab. 2009 Mar 3;
    Authors: Chen J, Cha-Molstad H, Szabo A, Shalev A
    Cardiomyocyte apoptosis is a critical process in the pathogenesis of ischemic and diabetic cardiomyopathy, but the mechanisms are not fully understood. Thioredoxin-interacting protein (TXNIP) has recently been shown to have deleterious effects in the cardiovascular system and we therefore investigated whether it may also play a role in diabetes-associated cardiomyocyte apoptosis. In fact, TXNIP expression was increased in H9C2 cardiomyocytes incubated at high glucose and cardiac expression of TXNIP and cleaved caspase-3 were also elevated in vivo in streptozotocin- ...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2238690</comments>
            <pubDate>Tue, 03 Mar 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2238690</guid>        </item>
        <item>
            <title>Estradiol Upregulates the Expression of Oxytocin Receptor in Colon in Rats.</title>
            <link>http://www.medworm.com/index.php?rid=2238689&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19258489%26dopt%3DAbstract</link>
            <description>Authors: Feng M, Qin JF, Wang C, Ye Y, Wang S, Xie DP, Wang PS, Liu C
    The study was designed to investigate the effect of estradiol (E2) on the excitatory effect of oxytocin on colon motility. Female Wistar rats were used and some of them were ovariectomized (OVX) and treated with E2. A plastic balloon made of condom was inserted into colon in order to monitor the change of colonic pressure in vivo. Longitudinal muscle strips of distal colon were prepared to monitored the spontaneous contraction of colon in vitro. Expression of oxytocin receptor (OTR) was investigated by Western blot analysis. Expression of OTR mRNA was detected by RT-PCR. Immunohistochemistry was used to locate OTR. In OVX rats, pretreatment of E2 (4-100 microg kg(-1), s.c.) dose dependently increased the excitatory e...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2238689</comments>
            <pubDate>Tue, 03 Mar 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2238689</guid>        </item>
        <item>
            <title>Interleukin-6 Activates Arginine-Vasopressin Neurons in the Supraoptic Nucleus during Immune Challenge in Rats.</title>
            <link>http://www.medworm.com/index.php?rid=2238688&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19258490%26dopt%3DAbstract</link>
            <description>This study aims at elucidating which factors underlie the activation of AVP neurons in response to immune stimulation mimicked by an intraperitoneal injection of lipopolysaccharide (LPS) in male Wistar rats. LPS treatment concomittanlty decreased diuresis and increased plasma AVP as well as AVP neuron activity in vivo, and these effects occurred as early as 30 min. Activation was sustained for more than six hours. Plasma osmolality did not change while blood pressure only transiently increased during the first hour post-LPS. PG-E2, IL-1beta and TNF-alpha mRNA expression raised 3 h after LPS, while IL-6 mRNA level increased 30 min post-LPS. In vivo electrophysiological recordings showed that brain IL-6 injection increased AVP neuron activity similarly to peripheral LPS treatment. In contras...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2238688</comments>
            <pubDate>Tue, 03 Mar 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2238688</guid>        </item>
        <item>
            <title>Brought in by force: AMPK, TBC1D1 and contraction-stimulated glucose transport in skeletal muscle.</title>
            <link>http://www.medworm.com/index.php?rid=2238687&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19258491%26dopt%3DAbstract</link>
            <description>Authors: Bilan PJ, Schertzer JD
    n/a.
    PMID: 19258491 [PubMed - as supplied by publisher] (Source: Am J Physiol Endocri...)</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2238687</comments>
            <pubDate>Tue, 03 Mar 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2238687</guid>        </item>
        <item>
            <title>Getting the Message Across- Mechanisms of Physiological Cross-Talk by Adipose Tissue.</title>
            <link>http://www.medworm.com/index.php?rid=2238686&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19258492%26dopt%3DAbstract</link>
            <description>Authors: Lee DE, Kehlenbrink S, Lee H, Hawkins MA, Yudkin JS
    Obesity is associated with resistance of skeletal muscle to insulin-mediated glucose uptake, as well as resistance of different organs and tissues to other metabolic and vascular actions of insulin. In addition, the body is exquisitely sensitive to nutrient imbalance, with energy excess or a high fat diet rapidly increasing insulin resistance even before noticeable changes occur in fat mass. There is a growing acceptance of the fact that, as well as acting as a storage site for surplus energy, adipose tissue is an important source of signals relevant to, inter alia, energy homeostasis, fertility and bone turnover. It has also been widely recognised that obesity is a state of low-grade inflammation, with adipose tissue generat...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2238686</comments>
            <pubDate>Tue, 03 Mar 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2238686</guid>        </item>
        <item>
            <title>Am J Physiol Endocrinol Metab; +29 new citations</title>
            <link>http://www.medworm.com/index.php?rid=2221176&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Fcmd%3DSearch%26db%3DPubMed%26term%3D%2528%2528%2528Am%2BJ%2BPhysiol%2BEndocrinol%2BMetab%2529%2BAND%2B%25222009%252F02%252F20%2B11%252E04%2522%255BMHDA%255D%253A%25222009%252F02%252F28%2B10%252E51%2522%255BMHDA%255D%2529%2529%2BNOT%2B%2528%2528%2B%2528%2528Am%2BJ%2BPhysiol%2BEndocrinol%2BMetab%255BTIAB%255D%2529%2529%2BAND%2B%25220001%2522%255BEDAT%255D%253A%25222009%252F02%252F20%2B11%252E04%2522%255BEDAT%255D%2529%2529</link>
            <description>29 new PubMed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Physiol Endocrinol Metab
These PubMed results were generated on 2009/02/28PubMed, a service of the National Library of Medicine, includes over 15 million 
citations for biomedical articles back to the 1950's.
These citations are from MEDLINE and additional life science journals. 
PubMed includes links to many sites providing full text articles and other related resources. (Source: Am J Physiol Endocri...)</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2221176</comments>
            <pubDate>Sat, 28 Feb 2009 15:51:47 +0100</pubDate>
            <guid isPermaLink="false">2221176</guid>        </item>
        <item>
            <title>Am J Physiol Endocrinol Metab; +30 new citations</title>
            <link>http://www.medworm.com/index.php?rid=2199050&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Fcmd%3DSearch%26db%3DPubMed%26term%3D%2528%2528%2528Am%2BJ%2BPhysiol%2BEndocrinol%2BMetab%2529%2BAND%2B%25222009%252F02%252F13%2B08%252E36%2522%255BMHDA%255D%253A%25222009%252F02%252F20%2B11%252E03%2522%255BMHDA%255D%2529%2529%2BNOT%2B%2528%2528%2B%2528%2528Am%2BJ%2BPhysiol%2BEndocrinol%2BMetab%255BTIAB%255D%2529%2529%2BAND%2B%25220001%2522%255BEDAT%255D%253A%25222009%252F02%252F13%2B08%252E36%2522%255BEDAT%255D%2529%2529</link>
            <description>30 new PubMed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Physiol Endocrinol Metab
These PubMed results were generated on 2009/02/20PubMed, a service of the National Library of Medicine, includes over 15 million 
citations for biomedical articles back to the 1950's.
These citations are from MEDLINE and additional life science journals. 
PubMed includes links to many sites providing full text articles and other related resources. (Source: Am J Physiol Endocri...)</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2199050</comments>
            <pubDate>Fri, 20 Feb 2009 16:03:57 +0100</pubDate>
            <guid isPermaLink="false">2199050</guid>        </item>
        <item>
            <title>Am J Physiol Endocrinol Metab; +36 new citations</title>
            <link>http://www.medworm.com/index.php?rid=2181413&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Fcmd%3DSearch%26db%3DPubMed%26term%3D%2528%2528%2528Am%2BJ%2BPhysiol%2BEndocrinol%2BMetab%2529%2BAND%2B%25222009%252F02%252F06%2B01%252E34%2522%255BMHDA%255D%253A%25222009%252F02%252F13%2B08%252E35%2522%255BMHDA%255D%2529%2529%2BNOT%2B%2528%2528%2B%2528%2528Am%2BJ%2BPhysiol%2BEndocrinol%2BMetab%255BTIAB%255D%2529%2529%2BAND%2B%25220001%2522%255BEDAT%255D%253A%25222009%252F02%252F06%2B01%252E34%2522%255BEDAT%255D%2529%2529</link>
            <description>36 new PubMed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Physiol Endocrinol Metab
These PubMed results were generated on 2009/02/13PubMed, a service of the National Library of Medicine, includes over 15 million 
citations for biomedical articles back to the 1950's.
These citations are from MEDLINE and additional life science journals. 
PubMed includes links to many sites providing full text articles and other related resources. (Source: Am J Physiol Endocri...)</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2181413</comments>
            <pubDate>Fri, 13 Feb 2009 13:35:30 +0100</pubDate>
            <guid isPermaLink="false">2181413</guid>        </item>
        <item>
            <title>GLUT8, the enigmatic intracellular hexose transporter.</title>
            <link>http://www.medworm.com/index.php?rid=2146889&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19176349%26dopt%3DAbstract</link>
            <description>Authors: Schmidt S, Joost HG, Schurmann A
    GLUT8 is a class III sugar transporter predominantly expressed in testis and brain. In contrast to the class I and class II transporters, hydrophobicity plots predict a short extracellular loop between transmembrane domain (TM) 1 and TM2 and a long extracellular loop between TM9 and TM10 that contains the only N-glycosylation site. In vitro translated GLUT8 migrates as a 35-kDa protein that is glycosylated in the presence of microsomal membranes. In heterologous expression systems, glucose transport activity (Km = 2 mM) was inhibited by fructose and galactose. The transporter carries an N-terminal endosomal/lysosomal targeting motif ([DE]XXXL[LI]). Accordingly, constitutive GLUT8 has been found to be associated with endosomes and lysosomes, but...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2146889</comments>
            <pubDate>Tue, 27 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2146889</guid>        </item>
        <item>
            <title>Maternal Obesity Down-Regulates Myogenesis and {beta}-Catenin Signaling in Fetal Skeletal Muscle.</title>
            <link>http://www.medworm.com/index.php?rid=2146888&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19176350%26dopt%3DAbstract</link>
            <description>In conclusion, our data showed that myogenesis and the Wnt/beta-catenin signaling pathway were down-regulated, whereas inflammatory IKK/NF-kappaB signaling pathways were up-regulated in fetal muscle of obese mothers. Key words: sheep, obesity, fetus, skeletal muscle.
    PMID: 19176350 [PubMed - as supplied by publisher] (Source: Am J Physiol Endocri...)</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2146888</comments>
            <pubDate>Tue, 27 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2146888</guid>        </item>
        <item>
            <title>Endurance swimming stimulates transepithelial calcium transport and alters the expression of genes related to calcium absorption in the intestine of rats.</title>
            <link>http://www.medworm.com/index.php?rid=2146887&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19176351%26dopt%3DAbstract</link>
            <description>In conclusion, endurance swimming enhanced intestinal calcium absorption, in part, by upregulating the calcium transporter genes. The present microarray study also provided relevant information for further investigations into the intestinal nutrient and electrolyte transport during non-impact exercise. Key words: gene ontology, microarray, non-impact exercise, real-time PCR, Ussing chamber.
    PMID: 19176351 [PubMed - as supplied by publisher] (Source: Am J Physiol Endocri...)</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2146887</comments>
            <pubDate>Tue, 27 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2146887</guid>        </item>
        <item>
            <title>Involvement of the Vitamin D Receptor in Energy Metabolism: Regulation of Uncoupling Proteins.</title>
            <link>http://www.medworm.com/index.php?rid=2146886&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19176352%26dopt%3DAbstract</link>
            <description>Authors: Wong KE, Szeto FL, Zhang W, Ye H, Kong J, Zhang Z, Sun XJ, Li YC
    Recent studies have established that vitamin D plays multiple biological roles beyond calcium metabolism; however, whether vitamin D is involved in energy metabolism is unknown. To address this question, we characterized the metabolic phenotypes of vitamin D receptor (VDR)-null mutant mice. Under a normocalcemic condition, VDR-null mice displayed less body fat mass and lower plasma triglyceride and cholesterol levels compared to wild-type (WT) mice; when placed on a high fat (HF) diet, VDR-null mice showed slower growth rate and accumulated less fat mass globally than WT mice, even though their food intake and intestinal lipid transport capacity were the same as WT mice. Consistent with the lower adipose mass, pl...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2146886</comments>
            <pubDate>Tue, 27 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2146886</guid>        </item>
        <item>
            <title>Human apolipoprotein D overexpression in transgenic mice induces insulin resistance and alters lipid metabolism.</title>
            <link>http://www.medworm.com/index.php?rid=2146885&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19176353%26dopt%3DAbstract</link>
            <description>Authors: Do Carmo S, Fournier D, Mounier C, Rassart E
    Apolipoprotein D (apoD), a widely expressed lipocalin, has the capacity to transport small hydrophobic molecules. Although it has been proposed that apoD may have multiple tissue-specific, physiological ligands and functions, these have yet to be identified. To gain insight in some of its functions, we generated transgenic mice overexpressing human apoD (H-apoD) under the control of neuron-specific promoters. In Thy-1/ApoD and NSE/ApoD mice, expression of H-apoD was strong in the nervous system although weakly detected in peripheral organs such as the liver and blood cells. These mice displayed not entirely anticipated metabolic defects. Although they are not obese and have normal lipid concentration in circulation, Thy-1/ApoD and N...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2146885</comments>
            <pubDate>Tue, 27 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2146885</guid>        </item>
        <item>
            <title>Berberine improves lipid dysregulation in obesity by controlling central and peripheral AMPK activity.</title>
            <link>http://www.medworm.com/index.php?rid=2146884&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19176354%26dopt%3DAbstract</link>
            <description>Authors: Kim WS, Lee YS, Cha SH, Jeong HW, Choe SS, Lee MR, Oh GT, Park HS, Lee KU, Lane D, Kim JB
    AMP-activated protein kinase (AMPK) plays an important role in regulating whole body energy homeostasis. Recently, we and others have reported that berberine (BBR) exerts anti-obesity and anti-diabetic effects in obese and diabetic rodent models through the activation of AMPK in peripheral tissues. Here we show that BBR improves lipid dysregulation and fatty liver in obese mice through central and peripheral actions. In obese db/db and ob/ob mice, BBR treatment reduced liver weight, and hepatic and plasma triglyceride and cholesterol contents. In liver and muscle of db/db mice, BBR promoted AMPK activity, fatty acid oxidation and changed expression of genes involved in lipid metabolism. A...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2146884</comments>
            <pubDate>Tue, 27 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2146884</guid>        </item>
        <item>
            <title>Estrogen receptor (ER){alpha}, ER{beta} and Aromatase knock-out effects on lower limb mass and contractile function in female mice.</title>
            <link>http://www.medworm.com/index.php?rid=2146883&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19176355%26dopt%3DAbstract</link>
            <description>Authors: Brown M, Ning J, Ferreira JA, Bogener JL, Lubahn DB
    Estrogen (E2) is reported to regulate skeletal muscle mass and contractile function; whether E2 exerts its effects through estrogen receptor alpha (ERalpha) or beta (ERbeta) is unclear. We determined the effect of ERalpha or ERbeta elimination on muscle mass and contractile function in multiple muscles of the lower limb, muscles with different locomotor tasks and proportions of fiber types I and II: soleus (Sol), plantaris (Plan), tibialis anterior (TA), and gastrocnemius (Gast), in mature female mice. To determine E2 elimination effects on muscle we also used Aromatase (Ar) knock-out (KO) and wild type (WT) mice. ERalpha and ArKO body weights were ~10 and 20% higher than WT. Although muscle mass tended to show a commensurate...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2146883</comments>
            <pubDate>Tue, 27 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2146883</guid>        </item>
        <item>
            <title>PET study of 11C-acetoacetate kinetics in rat brain during dietary treatments affecting ketosis.</title>
            <link>http://www.medworm.com/index.php?rid=2146882&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19176356%26dopt%3DAbstract</link>
            <description>Authors: Bentourkia M, Tremblay S, Pifferi F, Rousseau J, Lecomte R, Cunnane S
    Normally the brain's fuel is glucose but during fasting it increasingly relies on ketones (beta-hydroxybutyrate, acetoacetate and acetone) produced in liver mitochondria from fatty acid beta-oxidation. Although moderately raised blood ketones produced on a very high fat ketogenic diet have important clinical effects on the brain, including reducing seizures, ketone metabolism by the brain is still poorly understood. The aim of the present work was to assess brain uptake of carbon-11 labeled acetoacetate ((11)C-acetoacetate) by positron emission tomography (PET) imaging in the intact, living rat. In order to vary plasma ketones, we used three dietary conditions: control diet (high carbohydrate; low plasma ket...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2146882</comments>
            <pubDate>Tue, 27 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2146882</guid>        </item>
        <item>
            <title>The role of the liver in glucose homeostasis in PI 3-kinase p85{alpha}-deficient mice.</title>
            <link>http://www.medworm.com/index.php?rid=2146881&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19176357%26dopt%3DAbstract</link>
            <description>Authors: Aoki K, Matsui J, Kubota N, Nakajima H, Iwamoto K, Takamoto I, Tsuji Y, Ohno A, Mori S, Tokuyama K, Murakami K, Asano T, Aizawa S, Tobe K, Kadowaki T, Terauchi Y
    Phosphoinositide 3-kinase (PI3K) p85alpha-deficient mice exhibited hypoglycemia as a result of increased insulin sensitivity and glucose uptake in peripheral tissues. Although PI3K is central to the metabolic actions of insulin, its mechanism of action in liver is not well understood. In the present study, we investigated hepatic insulin signaling and glucose homeostasis in p85alpha-deficient and wild-type mice. In the livers of p85alpha-deficient mice, p50alpha played a compensatory role in insulin-stimulated PI3K activation by binding to IRS-1/2. In p85alpha-deficient mice, the ratio of p50alpha over p110 catalytic ...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2146881</comments>
            <pubDate>Tue, 27 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2146881</guid>        </item>
        <item>
            <title>New insights in covalent modifications of proteins and lipids: phosphorylation and beyond.</title>
            <link>http://www.medworm.com/index.php?rid=2146880&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19176358%26dopt%3DAbstract</link>
            <description>Authors: Marette A
    n/a.
    PMID: 19176358 [PubMed - as supplied by publisher] (Source: Am J Physiol Endocri...)</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2146880</comments>
            <pubDate>Tue, 27 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2146880</guid>        </item>
        <item>
            <title>Am J Physiol Endocrinol Metab; +30 new citations</title>
            <link>http://www.medworm.com/index.php?rid=2100375&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Fcmd%3DSearch%26db%3DPubMed%26term%3D%2528%2528%2528Am%2BJ%2BPhysiol%2BEndocrinol%2BMetab%2529%2BAND%2B%25222009%252F01%252F09%2B01%252E23%2522%255BMHDA%255D%253A%25222009%252F01%252F14%2B00%252E49%2522%255BMHDA%255D%2529%2529%2BNOT%2B%2528%2528%2B%2528%2528Am%2BJ%2BPhysiol%2BEndocrinol%2BMetab%255BTIAB%255D%2529%2529%2BAND%2B%25220001%2522%255BEDAT%255D%253A%25222009%252F01%252F09%2B01%252E23%2522%255BEDAT%255D%2529%2529</link>
            <description>30 new PubMed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Physiol Endocrinol Metab
These PubMed results were generated on 2009/01/14PubMed, a service of the National Library of Medicine, includes over 15 million 
citations for biomedical articles back to the 1950's.
These citations are from MEDLINE and additional life science journals. 
PubMed includes links to many sites providing full text articles and other related resources. (Source: Am J Physiol Endocri...)</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2100375</comments>
            <pubDate>Wed, 14 Jan 2009 05:49:31 +0100</pubDate>
            <guid isPermaLink="false">2100375</guid>        </item>
        <item>
            <title>Shotgun Lipidomics of Neutral Lipids as an Enabling Technology for Elucidation of Lipid-Related Diseases.</title>
            <link>http://www.medworm.com/index.php?rid=2089256&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19126783%26dopt%3DAbstract</link>
            <description>Authors: Gross RW, Han X
    Neutral lipids fulfill multiple specialized roles in cellular function. These roles include energy storage and utilization, the synthesis of complex lipids in cellular membranes, lipid second messengers for cellular signaling and the modulation of membrane molecular dynamics. We have developed a novel mass spectrometric technology, now termed shotgun lipidomics, that can identify the types and amounts of thousands of lipids directly from extracts of biologic samples. Shotgun lipidomics is well-suited for the identification and measurement of the types and amounts of neutral lipid classes and individual molecular species through the use of multidimensional mass spectrometry. This review summarizes the basic principles underlying the use of shotgun lipidomics for...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2089256</comments>
            <pubDate>Tue, 06 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2089256</guid>        </item>
        <item>
            <title>20-Hydroxyecdysone decreases weight and hyperglycemia in a diet-induced obesity mice model.</title>
            <link>http://www.medworm.com/index.php?rid=2089255&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19126784%26dopt%3DAbstract</link>
            <description>Authors: Kizelsztein P, Govorko D, Komarnytsky S, Evans A, Wang Z, Cefalu WT, Raskin I
    The steroid hormone 20-hydroxyecdysone (20HE) is an essential signaling molecule that modulates molting response in insects and may function as a putative anabolic factor in vertebrate animals, although no mammalian 20HE receptor has been identified. Here we show that in H4IIE cell culture, 20HE treatment decreased expression of phosphoenolpyruvate carboxykinase (PEPCK) and glucose-6-phosphatase (G6Pase), reduced glucose production, and induced Akt2 phosphorylation sensitive to the phosphoinositide-3 kinase (PI-3K) pathway specific inhibitor LY-294002. Daily oral administration of 20HE (10 mg/kg for 13 weeks) ameliorated obesity and insulin resistance in C57BL/6J mice fed a high-fat diet and produced...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2089255</comments>
            <pubDate>Tue, 06 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2089255</guid>        </item>
        <item>
            <title>Intracellular trafficking of the human oxytocin receptor: evidence of receptor recycling via a Rab4/Rab5 &quot;short cycle&quot;</title>
            <link>http://www.medworm.com/index.php?rid=2089254&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19126785%26dopt%3DAbstract</link>
            <description>We examined receptor resensitisation by first using HEK293T cells stably expressing human OTRs. Upon agonist activation, the receptors were almost completely sequestered inside intracellular compartments that were not labelled by lysosomal markers, thus indicating that the internalised receptors were not sorted to these degrading organelles. Binding and fluorescence assays showed that almost 85% of the receptors had returned to the cell surface after four hours, by which time cell responsiveness to the agonist was also completely restored, as shown by measuring phospholipase C (PLC) activation. Similar results were also obtained in the presence of cycloheximide, thus indicating that receptor recycling and not de novo receptor synthesis was responsible for the resensitisation. Notably, very...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2089254</comments>
            <pubDate>Tue, 06 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2089254</guid>        </item>
        <item>
            <title>Estrogen Replacement Enhances EDHF-Mediated Vasodilation of Mesenteric and Uterine Resistance Arteries: the Role of Endothelial Cell Ca2+</title>
            <link>http://www.medworm.com/index.php?rid=2089253&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19126786%26dopt%3DAbstract</link>
            <description>This study explores the role of estrogen in controlling EDHF-mediated vasodilation of resistance uterine arteries of the rat and also analyzes the contribution of endothelial cell Ca(2+) signaling to this process. A parallel study was also performed using mesenteric arteries to provide comparison with a non-reproductive vasculature. Mature female rats underwent ovariectomy, with one-half receiving 17ss-estradiol replacement (OVX+E) and the other half serving as estrogen-deficient controls (OVX). Uterine or mesenteric resistance arteries were harvested, cannulated, and pressurized. NO and prostacyclin production were inhibited with 200 microM LNNA and 10 microM indomethacin, respectively. ACh effectively dilated the arteries pre-constricted with phenylephrine, but failed to induce dilatatio...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2089253</comments>
            <pubDate>Tue, 06 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2089253</guid>        </item>
        <item>
            <title>Effects of intrafetal IGF-I on growth of cardiac myocytes in the late gestation fetal sheep.</title>
            <link>http://www.medworm.com/index.php?rid=2089252&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19126787%26dopt%3DAbstract</link>
            <description>In conclusion, the greater sizes and larger proportion of binucleated cardiac myocytes in female fetal sheep suggests that myocyte maturation may occur earlier in females than in males. This may explain in part the male sex specific responsiveness of cardiac hypertrophy to IGF-I in late gestation. If IGF-I stimulated cardiomyocyte growth is accompanied by maturation of contractile function, IGF-I may be a potential therapeutic agent for maintaining cardiac output in preterm males. Key words: IGF-I, fetal, hypertrophy, sex, heart.
    PMID: 19126787 [PubMed - as supplied by publisher] (Source: Am J Physiol Endocri...)</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2089252</comments>
            <pubDate>Tue, 06 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2089252</guid>        </item>
        <item>
            <title>Beyond Triglyceride Synthesis: The Dynamic Functional Roles of MGAT and DGAT Enzymes in Energy Metabolism.</title>
            <link>http://www.medworm.com/index.php?rid=2072486&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19116371%26dopt%3DAbstract</link>
            <description>Authors: Shi Y, Cheng D
    Monoacyglycerol acyltransferases (MGATs) and diacylglycerol acyltransferases (DGATs) catalyze two consecutive steps of enzyme reactions in the synthesis of triacylglycerols (TAGs). The metabolic complexity of TAG synthesis is reflected by the presence of multiple isoforms of MGAT and DGAT enzymes that differ in catalytic properties, subcellular localization, tissue distribution, and physiological functions. MGAT and DGAT enzymes play fundamental roles in the metabolism of monoacylglycerol (MAG), diacylglycerol (DAG), and triacylglycerol (TAG) that involved in many aspects of physiological functions, such as intestinal fat absorption, lipoprotein assembly, adipose tissue formation, signal transduction, satiety, and lactation. The recent progress in the phenotypic...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2072486</comments>
            <pubDate>Tue, 30 Dec 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2072486</guid>        </item>
        <item>
            <title>The genetics of neutral lipid biosynthesis, an evolutionary perspective.</title>
            <link>http://www.medworm.com/index.php?rid=2072485&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19116372%26dopt%3DAbstract</link>
            <description>Authors: Turkish AR, Sturley SL
    The storage of fatty acids and fatty alcohols in the form of neutral lipids such as triacylglycerol (TAG), cholesteryl ester (CE) and wax ester (WE) serves to provide reservoirs for membrane formation and maintenance, lipoprotein trafficking, lipid detoxification, evaporation barriers and for fuel in times of stress or nutrient deprivation. This ancient process likely originated in actinomycetes and has persisted in eukaryotes, albeit by different molecular mechanisms. A surfeit of neutral lipids is strongly, perhaps causally, related to several human diseases such as diabetes mellitus, obesity, atherosclerosis and non-alcoholic fatty liver disease. Therefore, understanding the metabolic pathways of neutral lipid synthesis and the roles of the enzymes in...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2072485</comments>
            <pubDate>Tue, 30 Dec 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2072485</guid>        </item>
        <item>
            <title>Benefits and limitations of reducing glucagon action for the treatment of type 2 diabetes.</title>
            <link>http://www.medworm.com/index.php?rid=2072484&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19116373%26dopt%3DAbstract</link>
            <description>Authors: Ali S, Drucker DJ
    Glucagon is secreted from the alpha cells of the pancreatic islets and regulates glucose homeostasis through modulation of hepatic glucose production. As elevated glucagon levels contribute to the pathophysiology of hyperglycemia in subjects with type 2 diabetes, reduction of glucagon receptor (Gcgr) activity represents a potential target for the treatment of T2DM. Herein we review current concepts of glucagon action in hepatic and extra-hepatic tissues and evaluate the therapeutic potential, mechanisms of action, and safety of reducing Gcgr signaling for the treatment of type 2 diabetes Key words: glucagon, insulin, liver, pancreas, diabetes.
    PMID: 19116373 [PubMed - as supplied by publisher] (Source: Am J Physiol Endocri...)</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2072484</comments>
            <pubDate>Tue, 30 Dec 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2072484</guid>        </item>
        <item>
            <title>3,5-diiodothyronine rapidly enhances mitochondrial fatty acid oxidation rate and thermogenesis in rat skeletal muscle: AMP-activated protein kinase involvement.</title>
            <link>http://www.medworm.com/index.php?rid=2072483&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19116374%26dopt%3DAbstract</link>
            <description>Authors: Lombardi A, de Lange P, Silvestri E, Busiello RA, Lanni A, Goglia F, Moreno M
    Triiodothyronine regulates energy metabolism and thermogenesis. Among triiodothyronine derivatives, 3,5-diiodo-L-thyronine (T2) has been shown to exert marked effects on energy metabolism by acting mainly at the mitochondrial level. Here we investigated the capacity of T2 to affect both skeletal muscle mitochondrial substrate oxidation and thermogenesis within 1 hour after its injection into hypothyroid rats. Administration of T2 induced an increase in mitochondrial oxidation when palmitoyl-CoA (+104%), palmitoyl-carnitine (+80%), or succinate (+30%) was used as substrate, but it had no effect when pyruvate was used. T2 was able a) to activate the AMPK-ACC-Malonyl CoA metabolic signalling pathway kno...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2072483</comments>
            <pubDate>Tue, 30 Dec 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2072483</guid>        </item>
        <item>
            <title>Hypothalamic proinflammatory lipid accumulation, inflammation, and insulin resistance in rats fed a high-fat diet.</title>
            <link>http://www.medworm.com/index.php?rid=2072482&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19116375%26dopt%3DAbstract</link>
            <description>Authors: Posey K, Clegg DJ, Printz RL, Byun J, Morton GJ, Vivekanandan-Giri A, Pennathur S, Baskin DG, Heinecke JW, Woods SC, Schwartz MW, Niswender KD
    Weight gain induced by an energy-dense diet is hypothesized to arise in part from defects in the neuronal response to circulating adiposity negative feedback signals, such as insulin. Peripheral tissue insulin resistance involves cellular inflammatory responses thought to be invoked by excess lipid. We sought to determine if similar signaling pathways are activated in the brain of rats fed a high-fat (HF) diet, and whether these effects depend upon excess calorie intake. We compared plasma hormones and glucose tolerance, behavioral and neuronal responses to intracerebroventricular (icv) insulin, hypothalamic long- chain acyl-CoA content...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2072482</comments>
            <pubDate>Tue, 30 Dec 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2072482</guid>        </item>
        <item>
            <title>Non-invasive Assessment of Pancreatic {beta} Cell Function In Vivo Using Manganese-Enhanced Magnetic Resonance Imaging.</title>
            <link>http://www.medworm.com/index.php?rid=2072481&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19116376%26dopt%3DAbstract</link>
            <description>Authors: Antkowiak PF, Tersey SA, Carter JD, Vandsburger MH, Nadler JL, Epstein FH, Mirmira RG
    The loss of beta cell function in Type 1 and Type 2 diabetes leads to metabolic dysregulation and an inability to maintain normoglycemia. The noninvasive imaging of beta cell function in vivo would therefore provide a valuable diagnostic and research tool for quantifying progression to diabetes and response to therapeutic intervention. Because manganese (Mn) is a T1-shortening magnetic resonance imaging (MRI) contrast agent that enters cells such as pancreatic beta cells through voltage-gated calcium channels, we hypothesized that Mn-enhanced MRI of the pancreas following glucose infusion would allow for non-invasive detection of beta cell function in vivo. To test this hypothesis, we adminis...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2072481</comments>
            <pubDate>Tue, 30 Dec 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2072481</guid>        </item>
        <item>
            <title>Fat for Life: New Stories on Old Grease.</title>
            <link>http://www.medworm.com/index.php?rid=2064634&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19106246%26dopt%3DAbstract</link>
            <description>Authors: Cheng D
    Editorial Focus, no abstract.
    PMID: 19106246 [PubMed - as supplied by publisher] (Source: Am J Physiol Endocri...)</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2064634</comments>
            <pubDate>Tue, 23 Dec 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2064634</guid>        </item>
        <item>
            <title>Adipose Triglyceride Lipase in human skeletal muscle is upregulated by exercise training.</title>
            <link>http://www.medworm.com/index.php?rid=2064633&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19106247%26dopt%3DAbstract</link>
            <description>Authors: Alsted TJ, Nybo L, Schweiger M, Fledelius C, Jacobsen P, Zimmermann R, Zechner R, Kiens B
    Mobilization of fatty acids from stored triacylglycerol (TG) in adipose tissue and skeletal muscle (intramyocellular triacylglycerol - IMTG) requires activity of lipases. Although exercise training increases the lipolytic capacity of skeletal muscle, the expression of hormone sensitive lipase (HSL) is not changed. Recently, adipose triglyceride lipase (ATGL) was identified as a TG specific lipase in various rodent tissues. To investigate whether human skeletal muscle ATGL protein is regulated by endurance exercise training, 10 healthy young men completed 8 weeks of supervised endurance exercise training. Western blotting analysis on lysates of skeletal muscle biopsy samples revealed that ...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2064633</comments>
            <pubDate>Tue, 23 Dec 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2064633</guid>        </item>
        <item>
            <title>ALCAT1 Is A Polyglycerophospholipid Acyltransferase Potently Regulated by Adenine Nucleotide and Thyroid Status.</title>
            <link>http://www.medworm.com/index.php?rid=2064632&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19106248%26dopt%3DAbstract</link>
            <description>Authors: Cao J, Shen W, Chang Z, Shi Y
    Acyl-CoA:lysocardiolipin acyltransferase-1 (ALCAT1) catalyzes acylation of lysocardiolipin back to cardiolipin, an important step involved in cardiolipin remodeling. The present study reports the catalytic properties of ALCAT1 in vitro and its regulation by thyroid hormone status in mouse liver and heart. The recombinant ALCAT1 expressed in Sf9 cells preferred basic pH conditions, and did not require divalent cations or the integrity of subcellular membrane for its enzymatic activity. The recombinant ALCAT1 was potently inhibited by ADP and ATP, but not by adenosine nucleotide analogues or other nucleotides such as UTP and GTP, suggesting that the ALCAT1 does not require ATP hydrolysis for its enzyme activity. In addition to cardiolipin, ALCAT1 al...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2064632</comments>
            <pubDate>Tue, 23 Dec 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2064632</guid>        </item>
        <item>
            <title>Incretin Release from Gut is Acutely Enhanced by Sugar but Not by Sweeteners In Vivo.</title>
            <link>http://www.medworm.com/index.php?rid=2064631&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19106249%26dopt%3DAbstract</link>
            <description>Authors: Fujita Y, Wideman RD, Speck M, Asadi A, King DS, Webber TD, Haneda M, Kieffer TJ
    Glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are released during meals from endocrine cells located in the gut mucosa and stimulate insulin secretion from pancreatic beta-cells in a glucose-dependent manner. Although the gut epithelium senses luminal sugars, the mechanism of sugar sensing and its downstream events coupled to the release of the incretin hormones are not clearly elucidated. Recently it was reported that sucralose, a sweetener that activates sweet receptors of taste buds, triggers incretin release from a murine enteroendocrine cell line in vitro. We confirmed that immunoreactivity of alpha-gustducin, a key G-coupled protein involved in taste ...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2064631</comments>
            <pubDate>Tue, 23 Dec 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2064631</guid>        </item>
        <item>
            <title>The effects of prolonged fasting and sustained lipolysis on insulin secretion and insulin sensitivity in normal subjects.</title>
            <link>http://www.medworm.com/index.php?rid=2064630&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19106250%26dopt%3DAbstract</link>
            <description>Authors: Salgin B, Marcovecchio ML, Humphreys SM, Hill N, Chassin LJ, Lunn DJ, Hovorka R, Dunger DB
    Normal betabeta-cells adjust their function to compensate for any decrease in insulin sensitivity. Our aim was to explore whether a prolonged fast would allow a study the effects of changes in circulating free fatty acid (FFA) levels on insulin secretion and insulin sensitivity, and whether any potential effects could be reversed by the anti-lipolytic agent Acipimox. 14 (8 female, 6 male) healthy young adults (aged 22.8-26.9 years) without a family history of diabetes and a BMI of 22.6+/-3.2 kg/m(2) were studied on three occasions in random order. Growth hormone and FFA levels were regularly measured overnight (22:00-07:59), and subjects underwent an intravenous glucose tolerance test (I...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2064630</comments>
            <pubDate>Tue, 23 Dec 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2064630</guid>        </item>
        <item>
            <title>Hormone Signaling Through Protein Destruction - A Lesson From Plants.</title>
            <link>http://www.medworm.com/index.php?rid=2010340&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19050175%26dopt%3DAbstract</link>
            <description>Authors: Tan X, Zheng N
    Ubiquitin-dependent protein degradation has emerged as a major pathway regulating eukaryotic biology. By employing a variety of ubiquitin ligases to target specific cellular proteins, the ubiquitin-proteasome system controls physiological processes in a highly regulated fashion. Recent studies on a plant hormone auxin have unveiled a novel paradigm of signal transduction, in which ubiquitin ligases function as hormone receptors. Perceived by the F-box protein subunit of the SCF-TIR1 ubiquitin ligase, auxin directly promotes the recruitment of a family of transcriptional repressors for ubiquitination, thereby activating extensive transcriptional programs. Structural studies have revealed that auxin functions through a &quot;molecular glue&quot; mechanism to enhance protein...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2010340</comments>
            <pubDate>Tue, 02 Dec 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2010340</guid>        </item>
        <item>
            <title>Enhanced cortisol production rates, free cortisol, and 11 Beta HSD1 expression correlate with visceral fat and insulin resistance in men: effect of weight loss.</title>
            <link>http://www.medworm.com/index.php?rid=2010339&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19050176%26dopt%3DAbstract</link>
            <description>Authors: Purnell JQ, Kahn SE, Samuels MH, Brandon D, Loriaux DL, Brunzell JD
    Controversy exists whether endogenous cortisol production is associated with visceral obesity and insulin resistance in humans. We therefore quantified cortisol production and clearance rates, abdominal fat depots, insulin sensitivity, and adipocyte gene expression in a cohort of 24 men. To test if found relationships are a consequence rather than a cause of obesity, 8 men from this larger group were studied before and after weight loss. Daily cortisol production rates (CPR), free hormone levels (FC), and metabolic clearance rates (MCR) were measured by stable isotope methodology and 24-hour sampling; intra-abdominal fat (IAF) and subcutaneous fat (SQF) by computed tomography; insulin sensitivity (SI) by frequ...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2010339</comments>
            <pubDate>Tue, 02 Dec 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2010339</guid>        </item>
        <item>
            <title>Renin dynamics in adipose tissue: adipose tissue control of local renin concentrations.</title>
            <link>http://www.medworm.com/index.php?rid=2010338&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19050177%26dopt%3DAbstract</link>
            <description>Authors: Fowler JD, Krueth SB, Bernlohr DA, Katz SA
    The renin angiotensin system (RAS) has been implicated in a variety of adipose tissue functions including tissue growth, differentiation, metabolism, and inflammation. While expression of all components necessary for a locally derived adipose tissue RAS have been demonstrated within adipose tissue, independence of local adipose RAS component concentrations from corresponding plasma RAS fluctuations has not been addressed. To analyze this, we varied in vivo rat plasma concentrations of two RAS components, renin and angiotensinogen (AGT), to determine the influence of their plasma concentrations on adipose and cardiac tissue levels in both perfused (plasma removed) and nonperfused samples. Variation of plasma RAS components was accompli...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2010338</comments>
            <pubDate>Tue, 02 Dec 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2010338</guid>        </item>
        <item>
            <title>Am J Physiol Endocrinol Metab; +30 new citations</title>
            <link>http://www.medworm.com/index.php?rid=1967754&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Fcmd%3DSearch%26db%3DPubMed%26term%3D%2528%2528%2528Am%2BJ%2BPhysiol%2BEndocrinol%2BMetab%2529%2BAND%2B%25222008%252F11%252F15%2B02%252E32%2522%255BMHDA%255D%253A%25222008%252F11%252F19%2B00%252E52%2522%255BMHDA%255D%2529%2529%2BNOT%2B%2528%2528%2B%2528%2528Am%2BJ%2BPhysiol%2BEndocrinol%2BMetab%255BTIAB%255D%2529%2529%2BAND%2B%25220001%2522%255BEDAT%255D%253A%25222008%252F11%252F15%2B02%252E32%2522%255BEDAT%255D%2529%2529</link>
            <description>30 new PubMed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

Am J Physiol Endocrinol Metab
These PubMed results were generated on 2008/11/19PubMed, a service of the National Library of Medicine, includes over 15 million 
citations for biomedical articles back to the 1950's.
These citations are from MEDLINE and additional life science journals. 
PubMed includes links to many sites providing full text articles and other related resources. (Source: Am J Physiol Endocri...)</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1967754</comments>
            <pubDate>Wed, 19 Nov 2008 05:52:08 +0100</pubDate>
            <guid isPermaLink="false">1967754</guid>        </item>
        <item>
            <title>Impact of Body Composition on Very-Low-Density-Lipoprotein-Triglycerides Kinetics.</title>
            <link>http://www.medworm.com/index.php?rid=1937786&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18984851%26dopt%3DAbstract</link>
            <description>Conclusion: Elevated VLDL-TG production without concomitant increased clearance via oxidation and adipose tissue redeposition contribute to hypertriglyceridemia in UBO women. Key words: VLDL-TG, Body composition, Obesity, Tracers, Fat biopsies.
    PMID: 18984851 [PubMed - as supplied by publisher] (Source: Am J Physiol Endocri...)</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1937786</comments>
            <pubDate>Tue, 04 Nov 2008 05:00:00 +0100</pubDate>
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            <title>Klotho Ablation Converts the Biochemical and Skeletal Alterations in FGF23 (R176Q) Transgenic Mice to a Klotho Deficient Phenotype.</title>
            <link>http://www.medworm.com/index.php?rid=1937785&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18984852%26dopt%3DAbstract</link>
            <description>In this study, we used a mouse genetic approach to validate in vivo the pivotal role of Klotho in the metabolic and skeletal derangements associated with FGF23 (R176Q) overexpression. To this end, we crossed mice heterozygous for the hypomorphic Klotho allele (Kl(+/-)) to F(Tg) mice and obtained F(Tg) transgenic mice homozygous for the Kl-hypomorphic allele (F(Tg)/Kl(-/-)). Mice were sacrificed on postnatal day 50 and serum and tissues were procured for analysis and comparison to F(Tg), WT, and Kl(-/-) controls. From 4 weeks onward, F(Tg)/Kl(-/-) mice were clearly distinguishable from F(Tg) mice and exhibited a striking phenotypic resemblance to the Kl(-/-) controls. Serum analysis for calcium, phosphorus, PTH, 1,25(OH)2D3, and ALP activity confirmed the biochemical similarity between the ...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1937785</comments>
            <pubDate>Tue, 04 Nov 2008 05:00:00 +0100</pubDate>
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        <item>
            <title>Methotrexate induces intestinal mucositis and alters gut protein metabolism independently of reduced food intake.</title>
            <link>http://www.medworm.com/index.php?rid=1937784&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18984853%26dopt%3DAbstract</link>
            <description>Authors: Boukhettala N, Leblond J, Claeyssens S, Faure M, Le Pessot F, B&amp;#xF4;le-Feysot C, Hassan A, Mettraux C, Vuichoud J, Lavoinne A, Breuill&amp;#xE9; D, D&amp;#xE9;chelotte P, Coeffier M
    One of the main secondary toxic side effects of antimitotic agents used to treat cancer patients is intestinal mucositis. This one is characterized by compromised digestive and absorptive functions, barrier integrity and immune competence. In the same time, food intake is decreased and may induce intestinal damages per se. The aim of the study was to characterize which alterations are specific to methotrexate, independently of the anorexic effect of the drug. Male Sprague-Dawley rats received subcutaneously saline solution as control group or 2.5 mg/kg of methotrexate during three days (D0-D2). Methotrexa...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1937784</comments>
            <pubDate>Tue, 04 Nov 2008 05:00:00 +0100</pubDate>
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            <title>Proteomic Changes associated with Diabetes in the BB-DP rat.</title>
            <link>http://www.medworm.com/index.php?rid=1937783&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18984854%26dopt%3DAbstract</link>
            <description>This study compared the protein expression of the liver, heart, and skeletal muscle of diabetic prone rats and matched controls utilizing semi-quantitative liquid chromatography mass spectrometry and differential in gel 2-D gel electrophoresis. Differential expression of 341proteins in liver, 43 in heart and 9 (2D gel only) in skeletal muscle were detected. These data were assembled into the relevant metabolic pathways affected primarily in liver. Multiple covalent modifications were also apparent in 2-D gel analysis. Several new hypotheses were generated by these data including mechanism of net cytosolic protein oxidation, formaldehyde generation by the methionine cycle, and inhibition of carbon substrate oxidation via reduction in citrate synthase and short chain acyl CoA dehydrogenase. ...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1937783</comments>
            <pubDate>Tue, 04 Nov 2008 05:00:00 +0100</pubDate>
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            <title>Pathways of Adipose Tissue Androgen Metabolism in Women: Depot Differences and Modulation by Adipogenesis.</title>
            <link>http://www.medworm.com/index.php?rid=1937782&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18984855%26dopt%3DAbstract</link>
            <description>In conclusion, higher mRNA levels of enzymes synthesizing and inactivating androgens are found in differentiated adipocytes, consistent with higher androgen processing rates in these cells. Glucocorticoid-induced androgen inactivation may locally modulate the exposure of adipose cells to active androgens. Key words: aldo-keto reductases, short chain dehydrogenases, adipocyte differentiation, omental, visceral fat.
    PMID: 18984855 [PubMed - as supplied by publisher] (Source: Am J Physiol Endocri...)</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1937782</comments>
            <pubDate>Tue, 04 Nov 2008 05:00:00 +0100</pubDate>
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            <title>Differences in partitioning of meal fatty acids into blood lipid fractions: a comparison of linoleate, oleate and palmitate.</title>
            <link>http://www.medworm.com/index.php?rid=1900104&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18940935%26dopt%3DAbstract</link>
            <description>Authors: Hodson L, McQuaid SE, Karpe F, Frayn KN, Fielding BA
    There has been much interest in the health effects of dietary fat but few studies have comprehensively compared the acute metabolic fate of specific fatty acids in vivo. We hypothesised that different classes of fatty acids would be variably partitioned in metabolic pathways and this would become evident over 24 h. We traced the fate of fatty acids using equal amounts of [U-(13)C]linoleate, [U-(13)C]oleate and [U-(13)C]palmitate given in a test breakfast meal in twelve healthy subjects. There was a tendency for differences in the concentrations of the tracers in plasma chylomicron-triacylglycerol (TG) (oleate &amp;gt; palmitate &amp;gt; linoleate). This pattern remained in plasma non-esterified fatty acid (NEFA) and very low-density...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1900104</comments>
            <pubDate>Tue, 21 Oct 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1900104</guid>        </item>
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            <title>Oxytocin Attenuates NADPH-Dependent Superoxide Activity and IL-6 Secretion in Macrophages and Vascular Cells.</title>
            <link>http://www.medworm.com/index.php?rid=1900103&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18940936%26dopt%3DAbstract</link>
            <description>Conclusions: These findings suggest oxytocin attenuates vascular oxidative stress and inflammation, two important pathophysiological processes in atherosclerosis. The fact that oxytocin receptors are found in monocytes and macrophages, and oxytocin decreases both superoxide production and release of a proinflammatory cytokine from these cells, suggests a potentially larger role for oxytocin in the attenuation of disease. Key words: oxytocin, macrophages, NADPH oxidase, interleukin-6, atherosclerosis.
    PMID: 18940936 [PubMed - as supplied by publisher] (Source: Am J Physiol Endocri...)</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1900103</comments>
            <pubDate>Tue, 21 Oct 2008 04:00:00 +0100</pubDate>
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