<?xml version="1.0" encoding="UTF-8"?>
<rss version="2.0">
    <channel>
        <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>Wed, 08 Feb 2012 15:08:48 +0100</lastBuildDate>
        <item>
            <title>Resistance training: the multifaceted side of exercise.</title>
            <link>http://www.medworm.com/index.php?rid=5643183&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%3D22275762%26dopt%3DAbstract</link>
            <description>Authors: Paoli A
    PMID: 22275762 [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=5643183</comments>
            <pubDate>Tue, 31 Jan 2012 10:36:20 +0100</pubDate>
            <guid isPermaLink="false">5643183</guid>        </item>
        <item>
            <title>Corrigendum.</title>
            <link>http://www.medworm.com/index.php?rid=5643182&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%3D22275763%26dopt%3DAbstract</link>
            <description>Authors: 
    PMID: 22275763 [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=5643182</comments>
            <pubDate>Tue, 31 Jan 2012 10:36:11 +0100</pubDate>
            <guid isPermaLink="false">5643182</guid>        </item>
        <item>
            <title>Am J Physiol Endocrinol Metab; +30 new citations</title>
            <link>http://www.medworm.com/index.php?rid=5625865&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%25222012%252F01%252F12%252016.24%2522%255BMHDA%255D%253A%25222012%252F01%252F25%252005.30%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%25222012%252F01%252F12%252016.24%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 2012/01/25PubMed, 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=5625865</comments>
            <pubDate>Wed, 25 Jan 2012 10:30:00 +0100</pubDate>
            <guid isPermaLink="false">5625865</guid>        </item>
        <item>
            <title>Dehydroepiandrosterone Reduces Preadipocyte Proliferation via Androgen Receptor.</title>
            <link>http://www.medworm.com/index.php?rid=5579982&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%3D22234368%26dopt%3DAbstract</link>
            <description>Authors: Fujioka K, Kajita K, Wu Z, Hanamoto T, Ikeda T, Mori I, Okada H, Yamauchi M, Uno Y, Morita H, Nagano I, Takahashi Y, Ishizuka T
    Abstract
    Several studies have suggested that both testosterone and dehydroepiandrosterone (DHEA) have weight-reducing and anti-diabetic effects especially in rodent studies; however, the precise mechanism of their action remains unclear. Here we investigated the effect of DHEA on cell growth in adipose tissue. The appearance of senescence-associated β-galactosidase in stromal vascular fraction (SVF) isolated from Otsuka Long-Evans Tokushima Fatty rats, an animal model of inherent obese type 2 diabetes, was prevented by DHEA administration. Next, the effects of DHEA and testosterone were compared in vivo and in vitro to evaluate whether these horm...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5579982</comments>
            <pubDate>Tue, 10 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5579982</guid>        </item>
        <item>
            <title>Overexpression of a short human seipin/BSCL2 isoform in mouse adipose tissue results in mild lipodystrophy.</title>
            <link>http://www.medworm.com/index.php?rid=5579981&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%3D22234369%26dopt%3DAbstract</link>
            <description>Authors: Cui X, Wang Y, Meng L, Fei W, Deng J, Xu G, Peng X, Ju S, Zhang L, Liu G, Zhao L, Yang H
    Abstract
    Berardinelli-Seip congenital lipodystrophy type 2 (BSCL2) is a recessive disorder characterized by an almost complete loss of adipose tissue, insulin resistance and fatty liver. BSCL2 is caused by loss-of-function mutations in the BSCL2/seipin gene, which encodes seipin. The essential role for seipin in adipogenesis has recently been established both in vitro and in vivo. However, seipin is highly upregulated at later stages of adipocyte development and its role in mature adipocytes remains to be elucidated. We have therefore generated transgenic mice overexpressing a short isoform of human BSCL2 gene (encoding 398 amino acids) using the adipocyte-specific aP2 promoter. The tr...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5579981</comments>
            <pubDate>Tue, 10 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5579981</guid>        </item>
        <item>
            <title>Potential interaction of brain natriuretic peptide with hyperadiponectinemia in preeclampsia.</title>
            <link>http://www.medworm.com/index.php?rid=5579980&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%3D22234370%26dopt%3DAbstract</link>
            <description>We examined the possible links between adiponectin and BNP in the pathophysiology of preeclampsia. We performed a cross-sectional study in 56 preeclampsia patients and 56 controls matched for gestational age and body mass index. The BNP, leptin and adiponectin levels were measured by ELISA, and their mRNA expressions were evaluated in omental adipose tissue by real-time PCR. The effects of BNP on adiponectin and leptin mRNA expression and secretion were investigated in primary cultures of adipocytes from obese and normal weight women. The BNP, adiponectin and leptin levels were significantly higher in preeclampsia patients compared with controls. The adiponectin level was significantly increased in normal weight preeclampsia patients compared with overweight preeclampsia patients. Adiponec...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5579980</comments>
            <pubDate>Tue, 10 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5579980</guid>        </item>
        <item>
            <title>SUMO down-regulates GLP-1 stimulated cAMP generation and insulin secretion.</title>
            <link>http://www.medworm.com/index.php?rid=5579979&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%3D22234371%26dopt%3DAbstract</link>
            <description>The objective of this study is to investigate down-regulation of GLP-1 signaling by Small Ubiquitin related MOdifier protein, (SUMO). Mouse islets exposed to high glucose showed increased expression of endogenous SUMO transcripts and its conjugating enzyme Ubc-9. Over-expression of SUMO-1 in MIN6 cells and primary mouse beta cells resulted in reduced static and real-time estimates of intracellular cAMP upon receptor stimulation with exendin-4, a GLP-1R agonist. GLP1-R was covalently modified by SUMO. Over-expression of SUMO-1 attenuated cell surface trafficking of GLP-1R which resulted in significantly reduced insulin secretion when stimulated by exendin-4, a GLP-1R agonist. Partial knock-down of SUMO conjugating enzyme Ubc-9 resulted in enhanced exendin-4 stimulated insulin secretion in m...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5579979</comments>
            <pubDate>Tue, 10 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5579979</guid>        </item>
        <item>
            <title>12/15-Lipoxygenase Signaling in the Endoplasmic Reticulum Stress Response.</title>
            <link>http://www.medworm.com/index.php?rid=5566732&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%3D22215650%26dopt%3DAbstract</link>
            <description>Authors: Cole BK, Kuhn NS, Green-Mitchell SM, Leone KA, Raab RM, Nadler JL, Chakrabarti SK
    Abstract
    Central obesity is associated with chronic inflammation, insulin resistance, β-cell dysfunction, and endoplasmic reticulum (ER) stress. The 12/15-lipoxygenase enzyme (12/15-LO) promotes inflammation and insulin resistance in adipose and peripheral tissues. Given that obesity is associated with ER stress and 12/15-LO is expressed in adipose tissue, we determined whether 12/15-LO could mediate ER stress signals. Addition of 12/15-LO lipid products, 12(S)-HETE and 12(S)-HPETE, to differentiated 3T3-L1 adipocytes induced expression and activation of ER stress markers, including BiP, XBP-1, P-PERK, and P-IRE1α. The ER stress inducer, tunicamycin, upregulated ER stress markers in adipocy...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5566732</comments>
            <pubDate>Tue, 03 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5566732</guid>        </item>
        <item>
            <title>Anabolic Signaling and Protein Deposition Are Enhanced by Intermittent as Compared with Continuous Feeding in Skeletal Muscle of Neonates.</title>
            <link>http://www.medworm.com/index.php?rid=5566731&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%3D22215651%26dopt%3DAbstract</link>
            <description>Authors: El-Kadi SW, Suryawan A, Gazzaneo MC, Srivastava N, Orellana RA, Nguyen HV, Lobley GE, Davis TA
    Abstract
    Orogastric tube feeding is indicated for neonates with impaired ability to ingest, and can be administered by intermittent bolus or continuous schedule. Our aim was to determine whether feeding modalities affect muscle protein deposition and to identify mechanisms involved. Neonatal pigs were overnight fasted (FAS) or fed the same amount of food continuously (CON) or intermittently (INT; 7 x 4 h meals) for 29 h. For 8 h, between hour 20 and 28, pigs were infused with [(2)H(5)]phenylalanine and [(2)H(2)]tyrosine and amino acid (AA) net balances were measured across the hindquarters. Insulin, branched-chain AA, phenylalanine and tyrosine arterial concentrations, and whole-...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5566731</comments>
            <pubDate>Tue, 03 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5566731</guid>        </item>
        <item>
            <title>Selective PPARγ Modulator INT131 Normalizes Insulin Signaling Defects and Improves Bone Mass in Diet-Induced Obese Mice.</title>
            <link>http://www.medworm.com/index.php?rid=5566715&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%3D22215652%26dopt%3DAbstract</link>
            <description>Authors: Lee DH, Huang H, Choi K, Mantzoros CS, Kim YB
    Abstract
    INT131 is a potent non-thiazolidinedione (TZD) selective peroxisome proliferators-activated receptor γ modulator being developed for the treatment of type 2 diabetes. In preclinical studies and a Phase II clinical trial, INT131 has been shown to lower glucose levels and ameliorate insulin resistance without typical TZD side effects. To determine whether the insulin-sensitizing action of INT131 is mediated by effects on insulin-mediated glucose homeostasis and insulin signaling, high-fat diet-induced obese (DIO), insulin-resistant mice treated with INT131 were studied. INT131's effects on bone density were also investigated. Treatment with INT131 enhanced systemic insulin sensitivity, as revealed by lower insulin level...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5566715</comments>
            <pubDate>Tue, 03 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5566715</guid>        </item>
        <item>
            <title>Plasma mannose binding lectin is stimulated by PPARα in humans.</title>
            <link>http://www.medworm.com/index.php?rid=5566714&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%3D22215653%26dopt%3DAbstract</link>
            <description>Authors: Rakhshandehroo M, Stienstra R, de Wit NJ, Bragt MC, Haluzik M, Mensink RP, Muller M, Kersten S
    Abstract
    The Peroxisome Proliferator Activated Receptor α (PPARα) is a major transcriptional regulator of lipid metabolism in liver and represents the molecular target for hypolipidemic fibrate drugs. Effects of PPARα on lipid metabolism are partially mediated by circulating proteins such as FGF21 and ANGPTL4. The present study was undertaken to screen for and identify circulating proteins produced by human liver that are under control of PPARα. Towards that aim, primary human hepatocytes were treated with the synthetic PPARα agonist Wy14643 and whole genome expression data selected for secreted proteins. Expression of FGF21, ANGPTL4 and mannose-binding lectin (MBL), a solub...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5566714</comments>
            <pubDate>Tue, 03 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5566714</guid>        </item>
        <item>
            <title>The role of the stomach in the control of appetite and the secretion of satiation peptides.</title>
            <link>http://www.medworm.com/index.php?rid=5566711&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%3D22215654%26dopt%3DAbstract</link>
            <description>THE ROLE OF THE STOMACH IN THE CONTROL OF APPETITE AND THE SECRETION OF SATIATION PEPTIDES.
    Am J Physiol Endocrinol Metab. 2012 Jan 3;
    Authors: Steinert RE, Meyer-Gerspach AC, Beglinger C
    Abstract
    It is widely accepted that gastric parameters such as gastric distention provide a direct negative feedback signal to inhibit eating; moreover, gastric and intestinal signals have been reported to synergize to promote satiation. There are, however, only few human data exploring the potential interaction effects of gastric and intestinal signals in the short-term control of appetite and the secretion of satiation peptides. We performed experiments in healthy subjects receiving either a rapid intragastric load or a continuous intraduodenal infusion of glucose or a mixed liquid meal....</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5566711</comments>
            <pubDate>Tue, 03 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5566711</guid>        </item>
        <item>
            <title>FoxO1 as a Double-edged Sword in the Pancreas: Analysis of Pancreas and β Cell-specific FoxO1 Knockout Mice.</title>
            <link>http://www.medworm.com/index.php?rid=5566707&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%3D22215655%26dopt%3DAbstract</link>
            <description>Authors: Kobayashi M, Kikuchi O, Sasaki T, Kim HJ, Yokota-Hashimoto H, Lee YS, Amano K, Kitazumi T, Susanti VY, Kitamura YI, Kitamura T
    Abstract
    Diabetes is characterized by an absolute or relative deficiency of pancreatic β cells. New strategies to accelerate β cell neogenesis or maintain existing β cells are desired for future therapies against diabetes. We previously reported that FoxO1 inhibits β cell growth through a Pdx1-mediated mechanism. However, we also reported that FoxO1 protects against β cell failure via the induction of NeuroD and MafA. Here, we investigate the physiological roles of FoxO1 in the pancreas by generating pancreas-specific (P-FoxO1-KO) and β cell-specific FoxO1 knockout mice (β-FoxO1-KO) and analyzing the metabolic parameters and pancreatic morph...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5566707</comments>
            <pubDate>Tue, 03 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5566707</guid>        </item>
        <item>
            <title>A perspective on the determination of mitochondrial biogenesis.</title>
            <link>http://www.medworm.com/index.php?rid=5552181&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%3D22205627%26dopt%3DAbstract</link>
            <description>Authors: Miller BF, Hamilton KL
    Abstract
    The measurement of mitochondrial biogenesis is important in the determination of aging and disease processes and the assessment of countermeasures to them. We argue that the frequently used assessments of cell signaling, mitochondrial protein mRNA, mitochondrial protein expression or enzyme activity, or mitochondrial density are not measurements that can lead to conclusions about mitochondrial biogenesis. Instead, we propose that only measures of mitochondrial synthesis are indicative of biogenesis. Clarification of this issue will hopefully result in further differentiation of the processes important for morphological and functional changes of mitochondria.
    PMID: 22205627 [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=5552181</comments>
            <pubDate>Wed, 28 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5552181</guid>        </item>
        <item>
            <title>A Major Prolactin Binding Complex on Human Milk Fat Globule Membranes Contains Cyclophilins A and B: The Complex is Not the Prolactin Receptor.</title>
            <link>http://www.medworm.com/index.php?rid=5552180&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%3D22205628%26dopt%3DAbstract</link>
            <description>Authors: Lorenson MY, Ueda EK, Chen KE, Walker AM
    Abstract
    Prolactin (PRL) in milk influences maturation of gastrointestinal epithelium and development of both the hypothalamo-pituitary and immune systems of offspring. Here, we demonstrate that most PRL in human milk is part of a novel, high affinity, multi-component binding complex found on the milk fat globule membrane and not in whey. To examine properties of the complex, a sensitive ELISA was developed such that human PRL (hPRL) binding to the complex was measured by loss of hPRL detectability; thus, as much as 50ng hPRL was undetectable in the presence of 10 µl human milk. Using the same methodology, no comparable complex formation was observed with human serum or amniotic fluid. hPRL complexation in milk was rapid, time depe...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5552180</comments>
            <pubDate>Wed, 28 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5552180</guid>        </item>
        <item>
            <title>Insight into molecular pathways of retinal metabolism, associated with vitellogenesis in zebrafish.</title>
            <link>http://www.medworm.com/index.php?rid=5552179&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%3D22205629%26dopt%3DAbstract</link>
            <description>Authors: Levi L, Ziv T, Admon A, Levavi-Sivan B, Lubzens E
    Abstract
    Retinal is the main retinoid stored in oviparous eggs of fish, amphibians and reptiles, reaching the oocytes in association with vitellogenins, the yolk precursor proteins. During early pre-segmentation stages of zebrafish embryos, retinal is metabolized to retinoic acid (RA) that regulates genes involved in cell proliferation, differentiation and tissue function, and is therefore essential for normal embryonic development. While synthesis of vitellogenin and its regulation by 17β-estradiol (E2) were extensively investigated, pathways for retinal synthesis remain obscure. We determined the expression pattern of 46 candidate genes aiming at identifying enzymes associated with retinal synthesis; ascertaining whether...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5552179</comments>
            <pubDate>Wed, 28 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5552179</guid>        </item>
        <item>
            <title>Contribution of FSH and triiodothyronine to the development of circadian clocks during granulosa cell maturation.</title>
            <link>http://www.medworm.com/index.php?rid=5552178&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%3D22205630%26dopt%3DAbstract</link>
            <description>Authors: Chu G, Misawa I, Chen H, Yamauchi N, Shigeyoshi Y, Hashimoto S, Hattori MA
    Abstract
    The involvement of FSH and triiodothyronine (T3) in the circadian clocks was investigated using immature granulosa cells of ovaries during the progress of cell maturation. The granulosa cells were prepared from preantral follicles of mouse Period2 (Per2)-dLuc reporter gene transgenic rats injected subcutaneously with a synthetic nonsteroidal estrogen diethylstilbestrol. The analysis of the cellular clock of the immature granulose cells was performed partly using a serum-free culture system. Several bioluminescence oscillations of Per2-dLuc promoter activity were generated in the presence of FSH + fetal bovine serum, but not in the presence of either FSH or serum. As revealed by bioluminesce...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5552178</comments>
            <pubDate>Wed, 28 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5552178</guid>        </item>
        <item>
            <title>Am J Physiol Endocrinol Metab; +73 new citations</title>
            <link>http://www.medworm.com/index.php?rid=5537410&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%25222011%252F11%252F19%252020.00%2522%255BMHDA%255D%253A%25222011%252F12%252F24%252020.18%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%25222011%252F11%252F19%252020.00%2522%255BEDAT%255D%29%29</link>
            <description>73 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 2011/12/24PubMed, 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=5537410</comments>
            <pubDate>Sun, 25 Dec 2011 01:18:01 +0100</pubDate>
            <guid isPermaLink="false">5537410</guid>        </item>
        <item>
            <title>Acute activation of central Glp1 receptors enhances hepatic insulin action and insulin secretion in high fat-fed, insulin resistant mice.</title>
            <link>http://www.medworm.com/index.php?rid=5426721&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%3D22094469%26dopt%3DAbstract</link>
            <description>Authors: Burmeister MA, Ferre T, Ayala JE, King EM, Holt RM, Ayala JE
    Abstract
    Glucagon-like peptide-1 (Glp1) receptor knockout (Glp1r-/-) mice exhibit impaired hepatic insulin action. High fat (HF)-fed Glp1r-/- mice exhibit improved, rather than the expected impaired, hepatic insulin action. This is due to decreased lipogenic gene expression and triglyceride accumulation. The present studies overcome these secondary adaptations by acutely modulating Glp1r action in HF-fed wild-type mice. The central Glp1r was targeted given its role as a regulator of hepatic insulin action. We hypothesized that acute inhibition of the central Glp1r impairs hepatic insulin action beyond the effects of HF feeding. We further hypothesized that activation of the central Glp1r improves hepatic insulin ...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5426721</comments>
            <pubDate>Tue, 15 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5426721</guid>        </item>
        <item>
            <title>Prolactin receptor antagonism in mouse anterior pituitary: effects on cell turnover and prolactin receptor expression.</title>
            <link>http://www.medworm.com/index.php?rid=5426720&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%3D22094470%26dopt%3DAbstract</link>
            <description>In conclusion, our observations suggest that prolactin is involved in the maintenance of physiological cell renewal in the anterior pituitary. Alterations in this physiological role of prolactin could contribute to pituitary tumor development.
    PMID: 22094470 [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=5426720</comments>
            <pubDate>Tue, 15 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5426720</guid>        </item>
        <item>
            <title>Proton magnetic resonance spectroscopy shows a lower intramyocellular lipid accumulation in middle-aged subjects predisposed to familial longevity.</title>
            <link>http://www.medworm.com/index.php?rid=5426719&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%3D22094471%26dopt%3DAbstract</link>
            <description>Conclusions. Offspring of nonagenarian siblings predisposed to longevity show lower IMCL levels compared to environmentally matched control subjects. Future research should focus on assessing what mechanisms may explain for the lower IMCL levels in familial longevity.
    PMID: 22094471 [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=5426719</comments>
            <pubDate>Tue, 15 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5426719</guid>        </item>
        <item>
            <title>Effects of Moderate Exercise on VLDL1 and Intralipid Kinetics in Overweight/Obese Middle-Aged Men.</title>
            <link>http://www.medworm.com/index.php?rid=5426718&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%3D22094472%26dopt%3DAbstract</link>
            <description>Authors: Al-Shayji IA, Caslake M, Gill JM
    Abstract
    Prior moderate exercise reduces plasma triglyceride (TG)-rich lipoprotein concentrations, mainly in the large very low density lipoprotein (VLDL(1)) fraction, but the mechanism responsible is unclear. We investigated the effects of brisk walking on TG-rich lipoprotein kinetics using a novel method. Twelve overweight/obese middle-aged men underwent two kinetic studies, involving infusion of Intralipid to block VLDL(1) catabolism, in random order. On the afternoon prior to infusion, subjects either walked on a treadmill for 2 hours at ~50% maximal oxygen uptake or performed no exercise. Multiple blood samples were taken during and post-infusion for separation of Intralipid (S(f) 400) and VLDL(1) (S(f) 60-400). VLDL(1)-TG and -apoB pr...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5426718</comments>
            <pubDate>Tue, 15 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5426718</guid>        </item>
        <item>
            <title>Oil composition of high fat diet affects differently metabolic inflammation in connection with endotoxin receptors in mice.</title>
            <link>http://www.medworm.com/index.php?rid=5426717&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%3D22094473%26dopt%3DAbstract</link>
            <description>Authors: Laugerette F, Furet JP, Debard C, Daira P, Loizon E, Geloen A, Soulage CO, Simonet C, Lefils-Lacourtablaise J, Bernoud-Hubac N, Bodennec J, Peretti N, Vidal H, Michalski MC
    Abstract
    Low-grade inflammation observed in obesity is a risk factor for cardiovascular disease. Recent studies revealed that this would be linked to gut-derived endotoxemia during fat digestion in high fat diets, but nothing is known about the effect of lipid composition. The study was designed to test the impact of oil composition of high fat diets on endotoxin metabolism and inflammation in mice. C57/Bl6 mice were fed for 8 weeks with chow or isocaloric isolipidic diets enriched with oils differing in fatty acid composition: milk fat, palm oil, rapeseed oil or sunflower oil. In vitro, adipocytes (3T3...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5426717</comments>
            <pubDate>Tue, 15 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5426717</guid>        </item>
        <item>
            <title>Am J Physiol Endocrinol Metab; +29 new citations</title>
            <link>http://www.medworm.com/index.php?rid=5382699&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%25222011%252F10%252F20%252013.40%2522%255BMHDA%255D%253A%25222011%252F11%252F07%252016.40%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%25222011%252F10%252F20%252013.40%2522%255BEDAT%255D%29%29</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 2011/11/07PubMed, 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=5382699</comments>
            <pubDate>Mon, 07 Nov 2011 21:40:02 +0100</pubDate>
            <guid isPermaLink="false">5382699</guid>        </item>
        <item>
            <title>Exercise with calorie restriction improves insulin sensitivity and glycogen synthase activity in obese post-menopausal women with impaired glucose tolerance.</title>
            <link>http://www.medworm.com/index.php?rid=5331988&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%3D22008454%26dopt%3DAbstract</link>
            <description>Conclusion: The greatest benefits at the whole body and cellular level (insulin activation of GS) in older women at highest risk for diabetes are derived from a lifestyle intervention including exercise and diet.
    PMID: 22008454 [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=5331988</comments>
            <pubDate>Tue, 18 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5331988</guid>        </item>
        <item>
            <title>Peripheral Oxytocin Suppresses Food Intake and Causes Weight Loss in Diet-Induced Obese Rats.</title>
            <link>http://www.medworm.com/index.php?rid=5331987&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%3D22008455%26dopt%3DAbstract</link>
            <description>Authors: Morton GJ, Thatcher BS, Reidelberger RD, Ogimoto K, Wolden-Hanson TH, Baskin DG, Schwartz MW, Blevins JE
    Abstract
    Growing evidence suggests that oxytocin plays an important role in the regulation of energy balance and that central oxytocin administration induces weight loss in diet-induced obese (DIO) animals. To gain a better understanding of how oxytocin mediates these effects, we examined feeding and neuronal responses to oxytocin in animals rendered obese following exposure to either a high-fat diet (HFD) or low-fat diet (LFD). Our findings demonstrate that peripheral administration of oxytocin dose-dependently reduces food intake and body weight to a similar extent in rats maintained on either diet. Moreover, the effect of oxytocin to induce weight loss remained intac...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5331987</comments>
            <pubDate>Tue, 18 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5331987</guid>        </item>
        <item>
            <title>Am J Physiol Endocrinol Metab; +22 new citations</title>
            <link>http://www.medworm.com/index.php?rid=5283234&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%25222011%252F09%252F29%252023.04%2522%255BMHDA%255D%253A%25222011%252F10%252F05%252001.24%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%25222011%252F09%252F29%252023.04%2522%255BEDAT%255D%29%29</link>
            <description>22 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 2011/10/05PubMed, 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=5283234</comments>
            <pubDate>Wed, 05 Oct 2011 05:24:53 +0100</pubDate>
            <guid isPermaLink="false">5283234</guid>        </item>
        <item>
            <title>Am J Physiol Endocrinol Metab; +26 new citations</title>
            <link>http://www.medworm.com/index.php?rid=5266546&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%25222011%252F09%252F20%252006.40%2522%255BMHDA%255D%253A%25222011%252F09%252F29%252023.04%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%25222011%252F09%252F20%252006.40%2522%255BEDAT%255D%29%29</link>
            <description>26 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 2011/09/29PubMed, 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=5266546</comments>
            <pubDate>Fri, 30 Sep 2011 03:04:54 +0100</pubDate>
            <guid isPermaLink="false">5266546</guid>        </item>
        <item>
            <title>Am J Physiol Endocrinol Metab; +32 new citations</title>
            <link>http://www.medworm.com/index.php?rid=5221182&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%25222011%252F09%252F01%252014.12%2522%255BMHDA%255D%253A%25222011%252F09%252F15%252014.19%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%25222011%252F09%252F01%252014.12%2522%255BEDAT%255D%29%29</link>
            <description>32 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 2011/09/15PubMed, 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=5221182</comments>
            <pubDate>Thu, 15 Sep 2011 18:19:58 +0100</pubDate>
            <guid isPermaLink="false">5221182</guid>        </item>
        <item>
            <title>Sunitinib induces Apoptosis in Pheochromocytoma Tumor Cells by Inhibiting VEGFR2/AKT/mTOR/S6K1 Pathways Through Modulation of Bcl-2 and BAD.</title>
            <link>http://www.medworm.com/index.php?rid=5180152&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%3D21878661%26dopt%3DAbstract</link>
            <description>Authors: Saito Y, Tanaka Y, Aita Y, Ishii KA, Ikeda T, Isobe K, Kawakami Y, Shimano H, Hara H, Takekoshi K
    Abstract
    Sunitinib is an oral multitargeted receptor tyrosine kinase inhibitor with antiangiogenic and antitumor activity that mainly targets vascular endothelial growth factor receptors (VEGFRs). Very recently, sunitinib has been shown to be an active agent for the treatment of malignant pheochromocytomas. However, it is unclear whether sunitinib acts only through an antiangiogenic mechanism or whether it may also directly target tumor cells. Sunitinib markedly induced apoptosis of PC12 cells in a dose-dependent and time-dependent manner. Further, in support of these findings, we found that sunitinib induced both a reduction in the expression of the anti-apoptotic molecule Bc...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5180152</comments>
            <pubDate>Mon, 29 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5180152</guid>        </item>
        <item>
            <title>Conditional Disruption of IGF-I Gene in Type 1{alpha}2-Collagen Expressing Cells Shows an Essential Role of IGF-I in Skeletal Anabolic Response to Loading.</title>
            <link>http://www.medworm.com/index.php?rid=5180151&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%3D21878662%26dopt%3DAbstract</link>
            <description>In conclusion, IGF-I expressed in type 1 collagen producing bone cells is critical for converting mechanical signal into anabolic signal in bone, and other growth factors cannot compensate for the loss of local IGF-I.
    PMID: 21878662 [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=5180151</comments>
            <pubDate>Mon, 29 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5180151</guid>        </item>
        <item>
            <title>Polyphenols, isothiocyanates and carotenoid derivatives enhance estrogenic activity in bone cells but inhibit it in breast cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=5180150&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%3D21878663%26dopt%3DAbstract</link>
            <description>Authors: Veprik A, Khanin M, Linnewiel Hermoni K, Danilenko M, Levy Y, Sharoni Y
    Abstract
    Exposure to estrogens is a major risk factor for breast and endometrial cancer. On the other hand, estrogens are beneficial for bone health. We have previously shown that carotenoids inhibit estrogen signaling in breast and endometrial cancer cells. The aim of this study was to compare the effects of various phytonutrients, (carotenoid derivatives, polyphenols, isothiocyanates) on estrogenic activity in breast cancer cells and osteoblast-like cells. All the tested phytonutrients inhibited estrogen response element (ERE) transactivation in breast cancer cells. However, these compounds either did not affect or even potentiate ERE activity and the expression of several bone-forming genes. These r...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5180150</comments>
            <pubDate>Mon, 29 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5180150</guid>        </item>
        <item>
            <title>A defect in Nrf2 signaling constitutes a mechanism for cellular stress hypersensitivity in type 2 diabetes.</title>
            <link>http://www.medworm.com/index.php?rid=5180149&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%3D21878664%26dopt%3DAbstract</link>
            <description>Authors: Bitar MS, Al-Mulla F
    Abstract
    NF-E2-related factor 2 (Nrf2) regulates the expression and coordinated induction of a battery of antioxidant phase 2 genes that protect aerobic cells against the cumulative damaging effects of oxidative stress (OS), which is a major contributor to the development of chronic diabetic complications. Using cultured dermal fibroblasts from patients with type 2 diabetes (DFs), we investigated the intracellular redox status and the adaptive response to OS, in which Nrf2 plays a central role. Our data confirmed that DFs exhibited hypersensitivity to hydrogen peroxide-induced necrotic cell death. Consistent with these findings, we also demonstrated a decrease in the intracellular level of ATP in DFs and a marked increase in the rate of release of pro-...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5180149</comments>
            <pubDate>Mon, 29 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5180149</guid>        </item>
        <item>
            <title>{beta}1-Adrenergic receptors increase UCP1 in human MADS brown adipocytes and rescue cold-acclimated {beta}3-adrenergic receptor KO mice via nonshivering thermogenesis.</title>
            <link>http://www.medworm.com/index.php?rid=5180148&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%3D21878665%26dopt%3DAbstract</link>
            <description>Authors: Mattsson CL, Csikasz RI, Chernogubova E, Yamamoto DL, Hogberg HT, Amri EZ, Hutchinson DS, Bengtsson T
    Abstract
    With the finding that brown adipose tissue is present and negatively correlated to obesity in adult man, finding the mechanism(s) of how to activate brown adipose tissue in humans could be important in combating obesity, type 2 diabetes, and their complications. In mice, the main regulator of nonshivering thermogenesis in brown adipose tissue is norepinephrine acting predominantly via β3-adrenergic receptors. However, vast majorities of β(3)-adrenergic agonists have so far not been able to stimulate human β3-adrenergic receptors or brown adipose tissue activity and it was postulated that human brown adipose tissue could be regulated instead by β(1)-adrenergic ...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5180148</comments>
            <pubDate>Mon, 29 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5180148</guid>        </item>
        <item>
            <title>Am J Physiol Endocrinol Metab; +38 new citations</title>
            <link>http://www.medworm.com/index.php?rid=5108356&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%25222011%252F07%252F26%252019.15%2522%255BMHDA%255D%253A%25222011%252F08%252F10%252001.45%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%25222011%252F07%252F26%252019.15%2522%255BEDAT%255D%29%29</link>
            <description>38 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 2011/08/10PubMed, 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=5108356</comments>
            <pubDate>Wed, 10 Aug 2011 05:45:02 +0100</pubDate>
            <guid isPermaLink="false">5108356</guid>        </item>
        <item>
            <title>Am J Physiol Endocrinol Metab; +16 new citations</title>
            <link>http://www.medworm.com/index.php?rid=5065077&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%25222011%252F07%252F12%252003.45%2522%255BMHDA%255D%253A%25222011%252F07%252F26%252019.15%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%25222011%252F07%252F12%252003.45%2522%255BEDAT%255D%29%29</link>
            <description>16 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 2011/07/26PubMed, 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=5065077</comments>
            <pubDate>Tue, 26 Jul 2011 23:15:12 +0100</pubDate>
            <guid isPermaLink="false">5065077</guid>        </item>
        <item>
            <title>Am J Physiol Endocrinol Metab; +33 new citations</title>
            <link>http://www.medworm.com/index.php?rid=5012058&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%25222011%252F06%252F26%252022.24%2522%255BMHDA%255D%253A%25222011%252F07%252F12%252003.45%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%25222011%252F06%252F26%252022.24%2522%255BEDAT%255D%29%29</link>
            <description>33 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 2011/07/12PubMed, 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=5012058</comments>
            <pubDate>Tue, 12 Jul 2011 07:45:02 +0100</pubDate>
            <guid isPermaLink="false">5012058</guid>        </item>
        <item>
            <title>Am J Physiol Endocrinol Metab; +21 new citations</title>
            <link>http://www.medworm.com/index.php?rid=4922276&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%25222011%252F05%252F29%252009.30%2522%255BMHDA%255D%253A%25222011%252F06%252F12%252013.30%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%25222011%252F05%252F29%252009.30%2522%255BEDAT%255D%29%29</link>
            <description>21 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 2011/06/12PubMed, 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=4922276</comments>
            <pubDate>Sun, 12 Jun 2011 17:30:02 +0100</pubDate>
            <guid isPermaLink="false">4922276</guid>        </item>
        <item>
            <title>Reply to letter to the editor: coronary flow velocity reserve was impaired in chronic hyperhomocysteinemic patients: why?</title>
            <link>http://www.medworm.com/index.php?rid=4876326&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%3D21613565%26dopt%3DAbstract</link>
            <description>Authors: Wang G, He L, Hong T
    
    PMID: 21613565 [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=4876326</comments>
            <pubDate>Sun, 29 May 2011 13:30:19 +0100</pubDate>
            <guid isPermaLink="false">4876326</guid>        </item>
        <item>
            <title>Insulin regulates its own delivery to skeletal muscle by feed-forward actions on the vasculature.</title>
            <link>http://www.medworm.com/index.php?rid=4876328&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%3D21610226%26dopt%3DAbstract</link>
            <description>Authors: Barrett EJ, Wang H, Upchurch C, Liu Z
    Insulin, at physiologic concentrations, regulates the volume of microvasculature perfused within skeletal and cardiac muscle. It can also, by relaxing the larger resistance vessels, increase total muscle blood flow. Both of these effects require endothelial cell nitric oxide generation and smooth muscle cell relaxation and each could increase delivery of insulin and nutrients to muscle. The capillary microvasculature possesses the greatest endothelial surface area of the body. Yet, whether insulin acts on the capillary endothelial cell is not known. Here we review insulin's actions at each of 3 levels of the arterial vasculature as well as recent data suggesting that insulin can regulate a vesicular transport system within the endothelial ...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4876328</comments>
            <pubDate>Mon, 23 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4876328</guid>        </item>
        <item>
            <title>Characterization of the Diurnal Rhythm of Peptide YY and its Association with Energy Balance Parameters in Normal Weight Premenopausal Women.</title>
            <link>http://www.medworm.com/index.php?rid=4876327&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%3D21610227%26dopt%3DAbstract</link>
            <description>CONCLUSION PYY displays a meal-driven diurnal rhythm and is correlated to RMR, a major contributor to energy expenditure. Thus, PYY varies in accordance with energy content and RMR, supporting a role for PYY in energy balance modulation.
    PMID: 21610227 [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=4876327</comments>
            <pubDate>Mon, 23 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4876327</guid>        </item>
        <item>
            <title>Postprandial Lipemia in Elderly Involves Increased Incorporation of Ingested Fat in Plasma Free Fatty Acids and Small (Sf 20-400) Triglyceride-rich Lipoproteins.</title>
            <link>http://www.medworm.com/index.php?rid=4823445&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%3D21558545%26dopt%3DAbstract</link>
            <description>Authors: Puga GM, Meyer C, Everman S, Mandarino LJ, Katsanos CS
    In elderly, the rise in postprandial plasma triglyceride (TG) concentrations is increased, contributing to their increased risk of cardiovascular disease. We sought to determine the incorporation of ingested fat (whipping cream enriched with [1,1,1-(13)C]-triolein) into plasma lipids during the postprandial period in six healthy elderly (67 ± 1 years old) and six healthy young (23 ± 2 years old) subjects. Blood and expired air samples were taken before, and at two-hour intervals during the 8-hour postprandial period. As expected, the area under the curve of postprandial plasma TG concentrations was larger in the elderly compared to the young subjects (152 ± 38 vs 66 ± 27 mg/dl×hr; P &amp;lt; 0.05). The incorporation of (1...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4823445</comments>
            <pubDate>Mon, 09 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4823445</guid>        </item>
        <item>
            <title>Skeletal Muscle Lipid Flux: Running Water Carries No Poison.</title>
            <link>http://www.medworm.com/index.php?rid=4823444&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%3D21558546%26dopt%3DAbstract</link>
            <description>Authors: Funai K, Semenkovich CF
    Lipids are the most abundant organic constituents in many humans. The rise in obesity prevalence has prompted a need for a more refined understanding of the effects of lipid molecules on cell physiology. In skeletal muscle, deposition of lipids can be associated with insulin resistance that contributes to the development of diabetes. Here we review the evidence that muscle cells are equipped with the molecular machinery to convert and sequester lipid molecules thus rendering them harmless. Induction of mitochondrial and lipogenic flux in the setting of elevated lipid deposition can protect muscle from lipid-induced &quot;poisoning&quot; of the cellular machinery. Lipid flux may also be directed towards the synthesis of ligands for nuclear receptors, further enhan...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4823444</comments>
            <pubDate>Mon, 09 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4823444</guid>        </item>
        <item>
            <title>Differential vascular damage in non-compensated versus compensated insulin resistance.</title>
            <link>http://www.medworm.com/index.php?rid=4823443&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%3D21558547%26dopt%3DAbstract</link>
            <description>Authors: Gomez-Hernandez A, de Las Heras N, Otero YF, Escribano O, Gozalbo-Lopez B, Guillen C, Cachofeiro V, Lahera V, Benito M
    The aim of this work was to study if the failure of the compensatory mechanisms in response to insulin resistance aggravates or its onset attenuates vascular damage. Thus, we analyzed the differential vascular damage induced by insulin resistance in obese brown adipose tissue insulin receptor knockout (BATIRKO) mice. BATIRKO mice show a decrease in interscapular brown fat mass and progressive glucose intolerance due to an insulin-secretion defect. Fed on high-fat diet, BATIRKO mice showed a significant increase of visceral adipose tissue mass versus body weight and insulin resistance as compared with controls. However, obese BATIRKO mice phenotyping revealed t...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4823443</comments>
            <pubDate>Mon, 09 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4823443</guid>        </item>
        <item>
            <title>Is Glutamine still an important precursor of citrulline?</title>
            <link>http://www.medworm.com/index.php?rid=4823442&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%3D21558548%26dopt%3DAbstract</link>
            <description>Authors: Ligthart-Melis GC, Deutz NE
    N/A.
    PMID: 21558548 [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=4823442</comments>
            <pubDate>Mon, 09 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4823442</guid>        </item>
        <item>
            <title>Altered contribution of rhoA/rho kinase signaling in contractile activity of myometrium in leptin receptor-deficient mice.</title>
            <link>http://www.medworm.com/index.php?rid=4823441&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%3D21558549%26dopt%3DAbstract</link>
            <description>Authors: Harrod JS, Rada CC, Pierce SL, England SK, Lamping KG
    In late gestation, enhanced myometrial contractility is mediated, in part, through increased rho/rho kinase. Since leptin, which is elevated in pregnancy and obesity, can directly depress myometrial function, we hypothesized that in leptin receptor-deficient mice, myometrial contractility would be greater in late pregnancy due to increased rho/rho kinase activity. To test this, we correlated rhoA and rho kinase expression to contractility in myometrium from non-pregnant (NP) and late-pregnant (P18) heterozygous leptin receptor-deficient mice (db/+) versus wild-type (WT) mice. In NP mice, KCl-induced contractions were similar between WT and db/+ myometrium. However, the rho kinase-dependent component of the contractions was ...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4823441</comments>
            <pubDate>Mon, 09 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4823441</guid>        </item>
        <item>
            <title>Differential Effects of Aging on Estrogen Negative and Positive Feedback.</title>
            <link>http://www.medworm.com/index.php?rid=4823440&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%3D21558550%26dopt%3DAbstract</link>
            <description>In conclusion, these studies in PMW demonstrate preservation of short-term steroid negative and positive feedback in response to exogenous E2 and P with aging. Attenuation of positive feedback in older compared to younger PMW is consistent with previous reports of declining GnRH responsiveness with aging.
    PMID: 21558550 [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=4823440</comments>
            <pubDate>Mon, 09 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4823440</guid>        </item>
        <item>
            <title>Am J Physiol Endocrinol Metab; +43 new citations</title>
            <link>http://www.medworm.com/index.php?rid=4768541&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%25222011%252F04%252F01%252005.45%2522%255BMHDA%255D%253A%25222011%252F04%252F30%252020.00%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%25222011%252F04%252F01%252005.45%2522%255BEDAT%255D%29%29</link>
            <description>43 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 2011/04/30PubMed, 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=4768541</comments>
            <pubDate>Sun, 01 May 2011 00:00:02 +0100</pubDate>
            <guid isPermaLink="false">4768541</guid>        </item>
        <item>
            <title>Spontaneously diabetic Ins2+/Akita:ApoE-deficient mice exhibit exaggerated hypercholesterolemia and atherosclerosis.</title>
            <link>http://www.medworm.com/index.php?rid=4663391&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%3D21447785%26dopt%3DAbstract</link>
            <description>In conclusion, exaggerated hypercholesterolemia and atherosclerosis in spontaneously diabetic Ins2(+/Akita):ApoE(-/-) mice may be attributable to impaired lipoprotein clearance in the setting of diminished expression of LSR and altered apolipoprotein composition of lipoproteins.
    PMID: 21447785 [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=4663391</comments>
            <pubDate>Mon, 28 Mar 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4663391</guid>        </item>
        <item>
            <title>The effect of sodium oxybate on growth hormone secretion in narcolepsy patients and healthy controls.</title>
            <link>http://www.medworm.com/index.php?rid=4663390&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%3D21447786%26dopt%3DAbstract</link>
            <description>In conclusion, SXB leads to a consistent increase in nocturnal GH secretion and strengthens the temporal relation between GH secretion and SWS. These data suggest that SXB may alter somatotropic tone in addition to its consolidating effect on nighttime sleep in narcolepsy. This could explain the suggested non-sleep effects of SXB, including body weight reduction.
    PMID: 21447786 [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=4663390</comments>
            <pubDate>Mon, 28 Mar 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4663390</guid>        </item>
        <item>
            <title>Am J Physiol Endocrinol Metab; +32 new citations</title>
            <link>http://www.medworm.com/index.php?rid=4603372&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%25222011%252F03%252F03%252010.45%2522%255BMHDA%255D%253A%25222011%252F03%252F17%252018.00%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%25222011%252F03%252F03%252010.45%2522%255BEDAT%255D%29%29</link>
            <description>32 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 2011/03/17PubMed, 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=4603372</comments>
            <pubDate>Thu, 17 Mar 2011 22:00:03 +0100</pubDate>
            <guid isPermaLink="false">4603372</guid>        </item>
        <item>
            <title>Am J Physiol Endocrinol Metab; +17 new citations</title>
            <link>http://www.medworm.com/index.php?rid=4541329&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%25222011%252F02%252F17%252009.15%2522%255BMHDA%255D%253A%25222011%252F03%252F03%252010.45%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%25222011%252F02%252F17%252009.15%2522%255BEDAT%255D%29%29</link>
            <description>17 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 2011/03/03PubMed, 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=4541329</comments>
            <pubDate>Thu, 03 Mar 2011 15:45:02 +0100</pubDate>
            <guid isPermaLink="false">4541329</guid>        </item>
        <item>
            <title>Am J Physiol Endocrinol Metab; +41 new citations</title>
            <link>http://www.medworm.com/index.php?rid=4483827&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%25222011%252F01%252F31%252013.00%2522%255BMHDA%255D%253A%25222011%252F02%252F17%252009.15%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%25222011%252F01%252F31%252013.00%2522%255BEDAT%255D%29%29</link>
            <description>41 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 2011/02/17PubMed, 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=4483827</comments>
            <pubDate>Thu, 17 Feb 2011 14:15:02 +0100</pubDate>
            <guid isPermaLink="false">4483827</guid>        </item>
        <item>
            <title>Corrigendum.</title>
            <link>http://www.medworm.com/index.php?rid=4416057&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%3D21270340%26dopt%3DAbstract</link>
            <description>Authors: 
    
    PMID: 21270340 [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=4416057</comments>
            <pubDate>Mon, 31 Jan 2011 18:00:13 +0100</pubDate>
            <guid isPermaLink="false">4416057</guid>        </item>
        <item>
            <title>Am J Physiol Endocrinol Metab; +42 new citations</title>
            <link>http://www.medworm.com/index.php?rid=4355031&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%25222010%252F12%252F24%252005.50%2522%255BMHDA%255D%253A%25222011%252F01%252F16%252019.45%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%25222010%252F12%252F24%252005.50%2522%255BEDAT%255D%29%29</link>
            <description>42 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 2011/01/16PubMed, 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=4355031</comments>
            <pubDate>Mon, 17 Jan 2011 00:45:03 +0100</pubDate>
            <guid isPermaLink="false">4355031</guid>        </item>
        <item>
            <title>Effect of exercise intensity and AICAR on isoform-specific expressions of murine skeletal muscle PGC-1{alpha} mRNA: a role of {beta}2-adrenergic receptor activation.</title>
            <link>http://www.medworm.com/index.php?rid=4205602&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%3D21098736%26dopt%3DAbstract</link>
            <description>In this study, effects of exercise intensity and 5-aminoimidazole-4-carboxamide-1β-D-ribofuranoside (AICAR) on isoform-specific expressions of PGC-1α were investigated. All isoforms were increased in proportion to exercise intensity of treadmill running (10-30 m/min for 30 min). Pre-injection of β2-adrenergic receptor (AR) antagonist (ICI 118551) inhibited the increase in PGC-1α-b and PGC-1α-c mRNAs but not the increase in PGC-1α-a mRNA in response to high-intensity exercise. Although high-intensity exercise activated α2-AMP-activated protein kinase (AMPK) in skeletal muscles, inactivation of α2-AMPK activity did not affect high-intensity exercise-induced mRNA expression of all PGC-1α isoforms, suggesting that activation of α2-AMPK is not mandatory for an increase in PGC-1α mRNA...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4205602</comments>
            <pubDate>Tue, 23 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4205602</guid>        </item>
        <item>
            <title>Organ-specific dietary fatty acid uptake in humans using positron emission tomography coupled to computed tomography.</title>
            <link>http://www.medworm.com/index.php?rid=4205601&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%3D21098737%26dopt%3DAbstract</link>
            <description>Authors: Labbé SM, Grenier-Larouche T, Croteau E, Normand-Lauzière F, Frisch F, Ouellet R, Guérin B, Turcotte EE, Carpentier AC
    A non-invasive method to determine postprandial fatty acid tissue partition may elucidate the link between excess dietary fat and type 2 diabetes. We hypothesized that the positron-emitting fatty acid analog 14(R,S)-[(18)F]-fluoro-6-thia-heptadecanoic acid ((18)FTHA) administered orally during a meal would be incorporated into chylomicron-triglycerides, allowing determination of inter-organ dietary fatty acid uptake. We administered (18)FTHA orally at the beginning of a standard liquid meal ingested in nine healthy men. There was no significant (18)FTHA uptake in the portal vein and the liver in the first hour. Whole body PET/CT acquisition revealed early a...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4205601</comments>
            <pubDate>Tue, 23 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4205601</guid>        </item>
        <item>
            <title>INSULIN-INDUCED SERINE PHOSPHORYLATION OF IRS-2 VIA ERK1/2 AND mTOR: STUDIES ON THE FUNCTION OF SER 675 AND SER 907.</title>
            <link>http://www.medworm.com/index.php?rid=4205600&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%3D21098738%26dopt%3DAbstract</link>
            <description>Authors: Fritsche L, Neukamm SS, Lehmann R, Kremmer E, Hennige AM, Hunder-Gugel A, Schenk M, Häring HU, Schleicher ED, Weigert C
    The identity of specific serine phosphorylation residues of insulin receptor substrate (IRS)-2 and their impact on insulin signal transduction are largely unknown. Ser 675 and Ser 907 of mouse IRS-2 are adjacent to PI3 kinase or Grb2 binding domains, respectively. Using monoclonal phospho-site specific antibodies we demonstrated the phosphorylation of both serines after stimulation of Fao hepatoma cells with insulin, anisomycin, or phorbol esters. Phosphorylation of both sites was a late and prolonged event during insulin treatment and was also detected in liver tissue of insulin-treated as well as refed mice. Inhibition and si-RNA mediated knockdown of ERK1...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4205600</comments>
            <pubDate>Tue, 23 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4205600</guid>        </item>
        <item>
            <title>Am J Physiol Endocrinol Metab; +22 new citations</title>
            <link>http://www.medworm.com/index.php?rid=4188058&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%25222010%252F11%252F12%252012.40%2522%255BMHDA%255D%253A%25222010%252F11%252F21%252021.15%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%25222010%252F11%252F12%252012.40%2522%255BEDAT%255D%29%29</link>
            <description>22 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 2010/11/21PubMed, 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=4188058</comments>
            <pubDate>Mon, 22 Nov 2010 02:15:02 +0100</pubDate>
            <guid isPermaLink="false">4188058</guid>        </item>
        <item>
            <title>Identification of a physiological role for leptin in the regulation of ambulatory activity and wheel running in mice.</title>
            <link>http://www.medworm.com/index.php?rid=4158864&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%3D21062956%26dopt%3DAbstract</link>
            <description>Authors: Morton GJ, Kaiyala KJ, Fischer JD, Ogimoto K, Schwartz MW, Wisse BE
    Mechanisms regulating spontaneous physical activity remain poorly characterized despite evidence of influential genetic and acquired factors. We evaluated ambulatory activity and wheel-running in leptin-deficient ob/ob mice, and in wild-type mice rendered hypoleptinemic by fasting, in both the presence and absence of subcutaneous leptin administration. In ob/ob mice, leptin treatment to plasma levels characteristic of wild-type mice acutely increased both ambulatory activity (by 4000±200 beam breaks/dark cycle, p&amp;lt;0.05) and total energy expenditure (TEE) (by 0.11±0.01kcal/hr during the dark cycle, p&amp;lt;0.05) in a dose-dependent manner and acutely increased wheel running (+350%, p&amp;lt;0.05). Fasting potently...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4158864</comments>
            <pubDate>Tue, 09 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4158864</guid>        </item>
        <item>
            <title>Regulation of adiponectin production by insulin: Interactions with tumor necrosis factor-alpha and interleukin-6.</title>
            <link>http://www.medworm.com/index.php?rid=4158863&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%3D21062957%26dopt%3DAbstract</link>
            <description>In conclusion, these studies show that insulin up-regulates adiponectin expression and release, and that TNF-αopposes the stimulatory effects of insulin. A combination between insulin resistance and increased TNF-α production could explain the decline of adiponectin level and isomer composition in plasma of obese insulin resistant subjects.
    PMID: 21062957 [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=4158863</comments>
            <pubDate>Tue, 09 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4158863</guid>        </item>
        <item>
            <title>Potential Therapeutic Role of Resistance Training in Diabetes: A Contribution by the 2009 Recipient of the APS New Investigator Award.</title>
            <link>http://www.medworm.com/index.php?rid=4158862&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%3D21062958%26dopt%3DAbstract</link>
            <description>Authors: Lang CH
    n/a.
    PMID: 21062958 [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=4158862</comments>
            <pubDate>Tue, 09 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4158862</guid>        </item>
        <item>
            <title>Role of the adipocyte-specific NF{kappa}B activity in the regulation of IP-10 and T cell migration.</title>
            <link>http://www.medworm.com/index.php?rid=4158861&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%3D21062959%26dopt%3DAbstract</link>
            <description>In conclusion, in this study we could demonstrate that the NFκB-pathway is essential for the regulation of IP-10 in 3T3-L1 and primary human adipocytes. Adipocytes rather than preadipocytes contribute to NFκB-dependent IP-10 expression and secretion. Furthermore, NFκB-dependent factors and especially IP-10 represent novel signals from adipocytes to induce T cell migration.
    PMID: 21062959 [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=4158861</comments>
            <pubDate>Tue, 09 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4158861</guid>        </item>
        <item>
            <title>Transaldolase Exchange and its Effects on Measurements of Gluconeogenesis in Humans.</title>
            <link>http://www.medworm.com/index.php?rid=4158860&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%3D21062960%26dopt%3DAbstract</link>
            <description>Conclusions: Substantial transaldolase exchange occurs in humans resulting in an overestimate of gluconeogenesis and an underestimate of glycogenolysis when measured with the (2)H(2)O method. Use of appropriate (13)C-tracers provides a means of correcting for transaldolase exchange.
    PMID: 21062960 [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=4158860</comments>
            <pubDate>Tue, 09 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4158860</guid>        </item>
        <item>
            <title>Am J Physiol Endocrinol Metab; +26 new citations</title>
            <link>http://www.medworm.com/index.php?rid=4141127&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%25222010%252F10%252F29%252012.50%2522%255BMHDA%255D%253A%25222010%252F11%252F07%252020.40%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%25222010%252F10%252F29%252012.50%2522%255BEDAT%255D%29%29</link>
            <description>26 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 2010/11/07PubMed, 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=4141127</comments>
            <pubDate>Mon, 08 Nov 2010 01:40:02 +0100</pubDate>
            <guid isPermaLink="false">4141127</guid>        </item>
        <item>
            <title>Enteral arginase ii provides ornithine for citrulline synthesis.</title>
            <link>http://www.medworm.com/index.php?rid=4109732&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%3D20978229%26dopt%3DAbstract</link>
            <description>ENTERAL ARGINASE II PROVIDES ORNITHINE FOR CITRULLINE SYNTHESIS.
    Am J Physiol Endocrinol Metab. 2010 Oct 26;
    Authors: Marini JC, Keller B, Cajo Didelija I, Castillo L, Lee B
    The synthesis of citrulline from arginine in the small intestine depends on the provision of ornithine. To test the hypothesis that arginase II plays a central role in the supply of ornithine for citrulline synthesis, the contribution of dietary arginine, glutamine and proline was determined utilizing multitracer stable isotope protocols in arginase II knockout (AII(-/-)) and wild type (WT) mice. The lack of arginase II resulted in a lower citrulline rate of appearance (121 vs.137 μmol•kg(-1)•h(-1)) due to a reduced availability of ornithine; ornithine supplementation, was able to restore the rate of c...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4109732</comments>
            <pubDate>Mon, 25 Oct 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4109732</guid>        </item>
        <item>
            <title>Adipose proinflammatory cytokine expression through sympathetic system is associated with hyperglycemia and insulin resistance in a rat ischemic stroke model.</title>
            <link>http://www.medworm.com/index.php?rid=4109731&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%3D20978230%26dopt%3DAbstract</link>
            <description>This study aimed to determine the effects of acute stroke on adipose inflammatory cytokine expression. In addition, because sympathetic activity is activated after acute stroke and catecholamines can regulate the expression of several adipocytokines, this study also evaluated whether alterations in adipose pro-inflammatory cytokines following acute stroke, if any, were medicated by sympathetic system. Acute ischemic brain injury was induced by ligating the right middle cerebral artery and bilateral common carotid arteries in male adult Sprague Dawley rats. Adipose TNF-α and monocyte chemoattractant protein 1 (MCP-1) mRNA and protein levels were determined by RT-PCR and enzyme-linked immunoassay, respectively. The stroke rats developed glucose intolerance on day 1 and 2 after cerebral isch...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4109731</comments>
            <pubDate>Mon, 25 Oct 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4109731</guid>        </item>
        <item>
            <title>Resveratrol recruits rat muscle microvasculature via a nitric oxide-dependent mechanism that is blocked by tumor necrosis factor-{alpha}</title>
            <link>http://www.medworm.com/index.php?rid=4109730&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%3D20978231%26dopt%3DAbstract</link>
            <description>In conclusion, resveratrol activates eNOS and increases muscle microvascular recruitment via an NO-dependent mechanism. Despite the potent antioxidant effect of resveratrol, TNF-α at concentrations that blocks insulin-mediated muscle microvascular recruitment completely neutralized resveratrol's microvascular action. Thus, chronic inflammation, as seen in type 2 diabetes, may limit resveratrol's vasodilatory actions on muscle microvasculature.
    PMID: 20978231 [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=4109730</comments>
            <pubDate>Mon, 25 Oct 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4109730</guid>        </item>
        <item>
            <title>APPL1 mediates adiponectin-stimulated p38 MAPK activation by scaffolding the TAK1-MKK3-p38 MAPK pathway.</title>
            <link>http://www.medworm.com/index.php?rid=4109729&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%3D20978232%26dopt%3DAbstract</link>
            <description>Authors: Xin X, Zhou L, Reyes CM, Liu F, Dong LQ
    The adaptor protein APPL1 mediates the stimulatory effect of adiponectin on p38 mitogen-activated protein kinase (MAPK) signaling, yet the underlying mechanism remains unclear. Here we show that in C2C12 cells, overexpression or suppression of APPL1 enhanced or suppressed, respectively, adiponectin-stimulated p38 MAPK upstream kinase cascade consisting of TGFβ-activated kinase 1 (TAK1) and mitogen-activated protein kinase kinase 3 (MKK3). In vitro affinity binding and co-immunoprecipitation experiments revealed that TAK1 and MKK3 bind to different regions of APPL1, suggesting that APPL1 functions as a scaffolding protein to facilitate adiponectin-stimulated p38 MAPK activation. Interestingly, suppressing APPL1 had no effect on TNFα-sti...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4109729</comments>
            <pubDate>Mon, 25 Oct 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4109729</guid>        </item>
        <item>
            <title>Cell cycle control of beta-cell replication in the prenatal and postnatal human pancreas.</title>
            <link>http://www.medworm.com/index.php?rid=4109728&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%3D20978233%26dopt%3DAbstract</link>
            <description>Conclusions: The strong expression of cyclin D3 in adult human beta-cells and its correlation to p27 and p16 suggest a positive role in human beta-cell cycle regulation. p16 and p27 appear to restrict beta-cell replication with ageing. The age-dependency of cell-cycle regulation in human beta-cells might explain the reduced beta-cell regeneration in adult humans.
    PMID: 20978233 [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=4109728</comments>
            <pubDate>Mon, 25 Oct 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4109728</guid>        </item>
        <item>
            <title>Evidence for Activation of Inflammatory Lipoxygenase Pathways in Visceral Adipose Tissue of Obese Zucker Rats.</title>
            <link>http://www.medworm.com/index.php?rid=4109727&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%3D20978234%26dopt%3DAbstract</link>
            <description>Authors: Chakrabarti SK, Wen Y, Dobrian AD, Cole BK, Ma Q, Pei H, Williams MD, Bevard MH, Vandenhoff GE, Keller SR, Gu J, Nadler JL
    Central obesity is associated with low grade inflammation which promotes type 2 diabetes and cardiovascular disease in obese individuals. The 12- and 5-lipoxygenase (12-LO and 5-LO) enzymes have been linked to inflammatory changes leading to the development of atherosclerosis. 12-LO has also been recently linked to inflammation and insulin resistance in adipocytes. We analyzed the expression of LO and pro-inflammatory cytokines in adipose tissue and adipocytes in obese Zucker rats, a widely studied genetic model of obesity, insulin resistance, and the metabolic syndrome. mRNA expression of 12-LO, 5-LO, and 5-LO activating protein (FLAP) were upregulated in...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4109727</comments>
            <pubDate>Mon, 25 Oct 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4109727</guid>        </item>
        <item>
            <title>Am J Physiol Endocrinol Metab; +23 new citations</title>
            <link>http://www.medworm.com/index.php?rid=4053532&amp;cid=s_33002_15_f&amp;fid=33002&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fsites%2Fentrez%26debug%3Dpubmeddembup%3Fcmd%3DSearch%26db%3Dpubmed%26term%3D%28%28%28Am%2520J%2520Physiol%2520Endocrinol%2520Metab%29%2520AND%2520%25222010%252F09%252F30%252017.50%2522%255BMHDA%255D%253A%25222010%252F10%252F10%252018.20%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%25222010%252F09%252F30%252017.50%2522%255BEDAT%255D%29%29</link>
            <description>23 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 2010/10/10PubMed, 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=4053532</comments>
            <pubDate>Sun, 10 Oct 2010 22:20:02 +0100</pubDate>
            <guid isPermaLink="false">4053532</guid>        </item>
        <item>
            <title>Am J Physiol Endocrinol Metab; +21 new citations</title>
            <link>http://www.medworm.com/index.php?rid=4017628&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%25222010%252F09%252F11%252018.12%2522%255BMHDA%255D%253A%25222010%252F09%252F30%252017.50%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%25222010%252F09%252F11%252018.12%2522%255BEDAT%255D%29%29</link>
            <description>21 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 2010/09/30PubMed, 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=4017628</comments>
            <pubDate>Thu, 30 Sep 2010 21:50:02 +0100</pubDate>
            <guid isPermaLink="false">4017628</guid>        </item>
        <item>
            <title>Am J Physiol Endocrinol Metab; +49 new citations</title>
            <link>http://www.medworm.com/index.php?rid=3958826&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%25222010%252F08%252F29%252014.39%2522%255BMHDA%255D%253A%25222010%252F09%252F11%252018.12%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%25222010%252F08%252F29%252014.39%2522%255BEDAT%255D%29%29</link>
            <description>49 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 2010/09/11PubMed, 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=3958826</comments>
            <pubDate>Sat, 11 Sep 2010 22:12:02 +0100</pubDate>
            <guid isPermaLink="false">3958826</guid>        </item>
        <item>
            <title>Am J Physiol Endocrinol Metab; +16 new citations</title>
            <link>http://www.medworm.com/index.php?rid=3903910&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%25222010%252F08%252F21%252001.45%2522%255BMHDA%255D%253A%25222010%252F08%252F26%252017.51%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%25222010%252F08%252F21%252001.45%2522%255BEDAT%255D%29%29</link>
            <description>16 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 2010/08/26PubMed, 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=3903910</comments>
            <pubDate>Thu, 26 Aug 2010 21:51:02 +0100</pubDate>
            <guid isPermaLink="false">3903910</guid>        </item>
        <item>
            <title>Androgen deprivation induces rapid involution and recovery of human prostate vasculature.</title>
            <link>http://www.medworm.com/index.php?rid=3858684&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%3D20699437%26dopt%3DAbstract</link>
            <description>ANDROGEN DEPRIVATION INDUCES RAPID INVOLUTION AND RECOVERY OF HUMAN PROSTATE VASCULATURE.
    Am J Physiol Endocrinol Metab. 2010 Aug 10;
    Authors: Godoy A, Montecinos VP, Gray DR, Sotomayor P, Yau JM, Vethanayagam RR, Singh S, Mohler JL, Smith GJ
    The response of the prostate tissue microenvironment to androgen deprivation (AD) represents a critical component in the treatment of benign prostatic hyperplasia and prostate cancer (CaP). Primary xenografts of human benign and CaP tissue transplanted to immunocompromised SCID mice were utilized to characterize the response of the prostate vasculature during the initial fourteen days of AD. Microvessel density and vascular lumen diameter in the prostate xenografts decreased rapidly after AD, reached a nadir on Days 2-4, and recovered betw...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3858684</comments>
            <pubDate>Mon, 09 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3858684</guid>        </item>
        <item>
            <title>Intense Acupuncture Normalizes Insulin Sensitivity, Increases Muscle GLUT4 Content, and Improves Lipid Profile in a Rat Model of Polycystic Ovary Syndrome.</title>
            <link>http://www.medworm.com/index.php?rid=3806854&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%3D20663984%26dopt%3DAbstract</link>
            <description>Authors: Johansson J, Yi F, Shao R, LÃ¶nn M, Billig H, Stener-Victorin E
    Polycystic ovary syndrome (PCOS) is associated with hyperandrogenism and insulin resistance, possibly reflecting defects in skeletal muscle and adipocyte insulin signaling. Low-frequency (2 Hz) electro-acupuncture (EA) increases insulin sensitivity in female rats with dihydrotestosterone (DHT)-induced PCOS, but the mechanism is unclear. We hypothesized that low-frequency EA regulates mediators involved in skeletal muscle glucose uptake and metabolism and alters the lipid profile in rats with DHT-induced PCOS. To test this hypothesis, we implanted in prepubescent female rats 90-d continuous-release pellets containing DHT (PCOS). At 70 d of age, the rats were randomly subdivided into two groups: one received low-f...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3806854</comments>
            <pubDate>Mon, 26 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3806854</guid>        </item>
        <item>
            <title>Sildenafil treatment in vivo stimulates Leydig cell steroidogenesis via cAMP and cGMP signaling pathway.</title>
            <link>http://www.medworm.com/index.php?rid=3806853&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%3D20663985%26dopt%3DAbstract</link>
            <description>This study was designed to assess the effects of prolonged sildenafil treatment on nitric oxide synthase (NOS)-dependent signaling and steroidogenic function of rat Leydig cells. Male adult rats were treated with Viagra (1.25 mg/kg body weight) daily, for 30 days. In our studies, serum testosterone and ex vivo testosterone production significantly increased in sildenafil-treated animals. Human chorionic gonadotropin (hCG)-stimulated testosterone production and cAMP accumulation were also significantly higher in Leydig cells obtained from sildenafil-treated rats. The expression of soluble guanylyl cyclase (GUCY1) subunits (Gucy1a1, Gucy1b1) significantly increased; cAMP specific Pde4a, cGMP specific Pde6c, dual Pde1c and Nos2, were inhibited and expression of Nos3, protein kinase 1 (Prkg1) ...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3806853</comments>
            <pubDate>Mon, 26 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3806853</guid>        </item>
        <item>
            <title>Fenofibrate promotes ischemia-induced revascularization through adiponectin-dependent pathway.</title>
            <link>http://www.medworm.com/index.php?rid=3806852&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%3D20663986%26dopt%3DAbstract</link>
            <description>Authors: Li P, Shibata R, Maruyama S, Kondo M, Ohashi K, Ouchi N, Murohara T
    Recent clinical trials demonstrated that PPARalpha agonist fenofibrate reduces cardiovascular events including limb amputation in people with type 2 diabetes. Here we investigated whether fenofibrate modulates the revascularization process in a mouse model of hindlimb ischemia. Treatment with fenofibrate led to acceleration of revascularization of ischemic hindlimb relative to the contralatereal limb in wild-type (WT) mice as measured by laser Doppler blood flow and capillary density analyses. Treatment of WT mice with fenofibrate increased the serum levels of adiponectin, which has protective actions on the vasculature. Of importance, fenofibrate had no effects on the revascularization in ischemic limbs of ad...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3806852</comments>
            <pubDate>Mon, 26 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3806852</guid>        </item>
        <item>
            <title>Role of urocortin 2 secreted by the pituitary in the stress-induced suppression of luteinizing hormone secretion in rats.</title>
            <link>http://www.medworm.com/index.php?rid=3806851&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%3D20663987%26dopt%3DAbstract</link>
            <description>Authors: Nemoto T, Iwasaki-Sekino A, Yamauchi N, Shibasaki T
    We have previously shown that urocortin 2 (Ucn 2), a member of the CRF peptide family, which binds to corticotropin releasing factor (CRF) type 2 receptor is expressed in proopiomelanocortin (POMC) cells of rat pituitary, and that its secretion and expression are increased by CRF in both the anterior and intermediate lobes and suppressed by glucocorticoids in the anterior lobe. We have also shown that Ucn 2 secreted by POMC cells acts on gonadotrophs expressing CRF type 2 receptors and inhibits the expression and secretion of gonadotropins. In the present study, we examined whether pituitary Ucn 2 is involved in stress-induced inhibition of gonadotropin secretion. A 90-minute-period of immobilization stress increased POMC mRN...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3806851</comments>
            <pubDate>Mon, 26 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3806851</guid>        </item>
        <item>
            <title>Glucagon and Lipid Interactions in the Regulation of Hepatic AMPK Signaling and Expression of PPAR{alpha} and FGF21 Transcripts in vivo.</title>
            <link>http://www.medworm.com/index.php?rid=3806850&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%3D20663988%26dopt%3DAbstract</link>
            <description>Authors: Berglund ED, Kang L, Lee-Young RS, Hansenour CM, Lustig DG, Lynes SG, Donahue EP, Swift LL, Charron MJ, Wasserman DH
    Hepatic glucagon action increases in response to accelerated metabolic demands and is associated with increased whole-body substrate availability including circulating lipids. The hypothesis that increases in hepatic glucagon action stimulate AMP-activated protein kinase (AMPK) signaling and peroxisome proliferator-activated receptor alpha (PPARalpha) and fibroblast growth factor 21 (FGF21) expression in a manner modulated by fatty acids was tested in vivo. Wild-type (gcgr(+/+)) and glucagon receptor-null (gcgr(-/-)) littermate mice were studied using an 18h fast, exercise, and hyperglucagonemic-euglycemic clamps +/- increased circulating lipids. Fasting and exe...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3806850</comments>
            <pubDate>Mon, 26 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3806850</guid>        </item>
        <item>
            <title>Am J Physiol Endocrinol Metab; +25 new citations</title>
            <link>http://www.medworm.com/index.php?rid=3781186&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%25222010%252F07%252F18%252001.24%2522%255BMHDA%255D%253A%25222010%252F07%252F23%252015.42%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%25222010%252F07%252F18%252001.24%2522%255BEDAT%255D%29%29</link>
            <description>25 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 2010/07/23PubMed, 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=3781186</comments>
            <pubDate>Fri, 23 Jul 2010 19:42:02 +0100</pubDate>
            <guid isPermaLink="false">3781186</guid>        </item>
        <item>
            <title>Am J Physiol Endocrinol Metab; +24 new citations</title>
            <link>http://www.medworm.com/index.php?rid=3762302&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%25222010%252F07%252F09%252015.06%2522%255BMHDA%255D%253A%25222010%252F07%252F18%252001.24%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%25222010%252F07%252F09%252015.06%2522%255BEDAT%255D%29%29</link>
            <description>24 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 2010/07/18PubMed, 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=3762302</comments>
            <pubDate>Sun, 18 Jul 2010 05:24:02 +0100</pubDate>
            <guid isPermaLink="false">3762302</guid>        </item>
        <item>
            <title>A critical appraisal of prevalence and metabolic significance of brown adipose tissue in adult humans.</title>
            <link>http://www.medworm.com/index.php?rid=3737811&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%3D20606075%26dopt%3DAbstract</link>
            <description>Authors: Lee P, Greenfield JR, Ho KK, Fulham MJ
    Brown adipose tissue (BAT) plays a major role in energy homeostasis in animals. Detection of BAT using Positron Emission Tomography (PET)-CT in humans has challenged the view that BAT disappears after infancy. Several recent studies, based on analysis of single scans, have reported a low prevalence of only 5-10% in humans, casting doubt on its significance. We undertook a critical analysis of the sensitivity, reproducibility and accuracy of PET-CT to deduce the prevalence of BAT and factors associated with its detection in adult humans. In a retrospective evaluation of PET-CT, using (18)F-fluodeoxyglucose, performed in 2934 patients, BAT was identified in 250 patients, yielding an apparent prevalence of 8.5%. Among these patients with BAT...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3737811</comments>
            <pubDate>Mon, 05 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3737811</guid>        </item>
        <item>
            <title>Palmitic Acid Acutely Inhibits Acetylcholine- but not GLP-1-Stimulated Insulin Secretion in Mouse Pancreatic Islets.</title>
            <link>http://www.medworm.com/index.php?rid=3737810&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%3D20606076%26dopt%3DAbstract</link>
            <description>Authors: Doliba NM, Qin W, Vinogradov SA, Wilson DF, Matschinsky FM
    Fatty acids, acetylcholine, and glucagon-like peptide (GLP-1) enhance insulin secretion in a glucose-dependent manner. However, the interplay between glucose, fatty acids, and the neuro-endocrine regulators of insulin secretion is not well understood. We therefore studied the acute effects of palmitic acid (PA) on isolated cultured mouse islets. Two different sets of experiments were designed: in one, a fixed concentration of 0.5 mM of PA bound to 0.15 mM bovine serum albumin (BSA) was used; in the other, a PA ramp from 0 to 0.5 mM was applied at fixed albumin concentration of 0.15 mM so that the molar PA/BSA ratio changed within the physiological range. At a fixed concentration of 0.5 mM, PA markedly inhibited acetylc...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3737810</comments>
            <pubDate>Mon, 05 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3737810</guid>        </item>
        <item>
            <title>Insulin resistance syndrome blunts the mitochondrial anabolic response following resistance exercise.</title>
            <link>http://www.medworm.com/index.php?rid=3737809&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%3D20606077%26dopt%3DAbstract</link>
            <description>Authors: Nilsson MI, Greene NP, Dobson JP, Wiggs MP, Gasier HG, Macias BR, Shimkus KL, Fluckey JD
    Metabolic risk factors associated with insulin resistance syndrome may attenuate augmentations in skeletal muscle protein anabolism following contractile activity. The purpose of the current study was to investigate whether or not the anabolic response, as defined by an increase in cumulative protein synthesis rates (24-h FSR) following resistance exercise (RE), is blunted in skeletal muscle of a well-established rodent model of insulin resistance syndrome. Four-month-old lean [Fa/?] and obese [fa/fa] Zucker rats engaged in four lower-body resistance exercise (RE) sessions over eight days, with the last bout occurring 16 h prior to muscle harvest. A flooding dose of deuterium oxide ((2)H(2...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3737809</comments>
            <pubDate>Mon, 05 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3737809</guid>        </item>
        <item>
            <title>Deletion of Nck1 attenuates hepatic ER stress signaling, improves glucose tolerance and insulin signaling in liver of obese mice.</title>
            <link>http://www.medworm.com/index.php?rid=3722581&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%3D20587749%26dopt%3DAbstract</link>
            <description>In this study, we report that the Src homology domain-containing adaptor protein Nck1, previously shown to modulate the UPR, is of functional importance in obesity-induced ER stress signaling and inhibition of insulin actions. We have examined obese Nck1(-/-) and Nck1(+/+) mice for glucose tolerance, insulin sensitivity and signaling, as well as for ER stress markers and IRS-1 phosphorylation at Ser(307). Our findings show that obese Nck1-deficient mice display improved glucose disposal accompanied by enhanced insulin signaling in liver. This correlates with attenuated IRE1alpha and JNK activation, and IRS-1 phosphorylation at Ser(307) compared to obese wild-type mice. Consistent with our in vivo data, we report that downregulation of Nck1 using siRNA in HepG2 cells results in decreased th...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3722581</comments>
            <pubDate>Mon, 28 Jun 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3722581</guid>        </item>
        <item>
            <title>Inconsistent formation and non function of insulin positive cells from pancreatic endoderm derived from human embryonic stem cells in athymic nude rats.</title>
            <link>http://www.medworm.com/index.php?rid=3722580&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%3D20587750%26dopt%3DAbstract</link>
            <description>Authors: Matveyenko AV, Georgia S, Bhushan A, Butler PC
    Embryonic stem cell therapy has been proposed as a therapeutic strategy to restore beta-cell mass and function in T1DM. Recently group from Novocell reported successful development of glucose-responsive islet like structures after implantation of pancreatic endoderm derived from human embryonic stem cells (hESC) into immune deficient mice. Our objective was to determine whether implantation of hESC derived pancreatic endoderm from Novocell into athymic nude rats results in development of viable glucose-responsive pancreatic endocrine tissue. Athymic nude rats were implanted with pancreatic endoderm (PE) derived from hESC either via implantation into the epididymal fat pads or by subcutaneous implantation into TheraCyte encapsulati...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3722580</comments>
            <pubDate>Mon, 28 Jun 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3722580</guid>        </item>
        <item>
            <title>Unsaturated fatty acids prevent desensitization of the human growth hormone secretagogue receptor by blocking its internalization.</title>
            <link>http://www.medworm.com/index.php?rid=3722579&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%3D20587751%26dopt%3DAbstract</link>
            <description>In conclusion, our findings demonstrate the importance of membrane composition for GHSR activation and desensitization, and indicate at least part of the mechanism through which OFAs and cholesterol could affect ghrelin's activity in vivo.
    PMID: 20587751 [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=3722579</comments>
            <pubDate>Mon, 28 Jun 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3722579</guid>        </item>
        <item>
            <title>Single-cell analysis of insulin-regulated fatty acid uptake in adipocytes.</title>
            <link>http://www.medworm.com/index.php?rid=3696297&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%3D20570821%26dopt%3DAbstract</link>
            <description>Authors: Varlamov O, Somwar R, Cornea A, Kievit P, Grove KL, Roberts CT
    Increased body fat correlates with the enlargement of average fat cell size and reduced adipose tissue insulin sensitivity. It is currently unclear if adipocytes, as they accumulate more triglycerides and grow in size, gradually become less insulin-sensitive, or if obesity-related factors independently cause both the enlargement of adipocyte size and reduced adipose tissue insulin sensitivity. In the first instance, large and small adipocytes in the same tissue would exhibit differences in insulin sensitivity, while, in the second, adipocyte size per se would not necessarily correlate with insulin response. To analyze the effect of adipocyte size on insulin sensitivity, we employed a new single-cell imaging assay t...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3696297</comments>
            <pubDate>Mon, 21 Jun 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3696297</guid>        </item>
        <item>
            <title>Insulin sensitive obesity.</title>
            <link>http://www.medworm.com/index.php?rid=3696296&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%3D20570822%26dopt%3DAbstract</link>
            <description>In conclusion, independently of total body fat mass, increased visceral fat accumulation and adipose tissue dysfunction are associated with IR obesity. This suggests that mechanisms beyond a positive caloric balance such as inflammation and adipokine release determine the pathological metabolic consequences in patients with obesity.
    PMID: 20570822 [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=3696296</comments>
            <pubDate>Mon, 21 Jun 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3696296</guid>        </item>
        <item>
            <title>Genetic, hormonal and metabolomic influences on social behavior and gender preference of xxy mice.</title>
            <link>http://www.medworm.com/index.php?rid=3696295&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%3D20570823%26dopt%3DAbstract</link>
            <description>GENETIC, HORMONAL AND METABOLOMIC INFLUENCES ON SOCIAL BEHAVIOR AND GENDER PREFERENCE OF XXY MICE.
    Am J Physiol Endocrinol Metab. 2010 Jun 22;
    Authors: Liu PY, Erkkila K, Lue Y, Jentsch JD, Schwarcz MD, Abuyounes D, Sinha Hikim AP, Wang C, Lee PW, Swerdloff RS
    XXY men (Klinefelter syndrome) are testosterone deficient, socially isolated, exhibit impaired gender identity and may experience more homosexual behaviors. Here we characterize social behaviors in a validated XXY mouse model to understand mechanisms. Sociability and gender preference were assessed by three-chambered choice tasks before, after castration, and after testosterone replacement. Metabolomic activities of brain and blood were quantified through fractional synthesis rates of palmitate and ribose (GC-MS). XXY mic...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3696295</comments>
            <pubDate>Mon, 21 Jun 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3696295</guid>        </item>
        <item>
            <title>Am J Physiol Endocrinol Metab; +30 new citations</title>
            <link>http://www.medworm.com/index.php?rid=3656960&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%25222010%252F06%252F05%252001.00%2522%255BMHDA%255D%253A%25222010%252F06%252F13%252012.21%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%25222010%252F06%252F05%252001.00%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 2010/06/13PubMed, 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=3656960</comments>
            <pubDate>Sun, 13 Jun 2010 16:21:02 +0100</pubDate>
            <guid isPermaLink="false">3656960</guid>        </item>
        <item>
            <title>Regulation of glucose-and mitochondrial fuel-induced insulin secretion by a cytosolic protein histidine phosphatase in pancreatic {beta}-cells.</title>
            <link>http://www.medworm.com/index.php?rid=3604019&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%3D20501872%26dopt%3DAbstract</link>
            <description>We report localization of a cytosolic protein histidine phosphatase (~ 16 kDa; PHP) in INS 832/13 cells, normal rat islets and human islets. siRNA-mediated knockdown of PHP markedly reduced glucose-or mitochondrial fuel-induced, but not KCl-induced insulin secretion. siRNA-mediated knockdown of PHP also attenuated mastoparan-induced insulin secretion suggesting its participation in G-protein-sensitive signaling steps leading to insulin secretion. Functional assays revealed that the beta-cell PHP catalyzes the dephosphorylation of ATP-citrate lyase (ACL). Silencing of PHP expression markedly reduced ACL activity suggesting functional regulation of ACL by PHP in beta-cells. Co-immunoprecipitation studies revealed modest effects of glucose on the interaction between PHP and ACL. Confocal micr...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3604019</comments>
            <pubDate>Mon, 24 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3604019</guid>        </item>
        <item>
            <title>Increased fat mass, decreased myofiber size, and a shift to glycolytic muscle metabolism in adolescent male transgenic mice overexpressing IGFBP-2.</title>
            <link>http://www.medworm.com/index.php?rid=3604018&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%3D20501873%26dopt%3DAbstract</link>
            <description>Authors: Rehfeldt C, Renne U, Sawitzky M, Binder G, Hoeflich A
    To elucidate the functional role of insulin-like growth factor (IGF)-binding protein-2 (IGFBP-2) for in vivo skeletal muscle growth and function, skeletal muscle cellularity and metabolism, expression of signal molecules, as well as body growth and composition were studied in a transgenic mouse model overexpressing IGFBP-2. Postnatal growth rate of transgenic mice was reduced from day 21 of age by 6-8% compared with non-transgenic controls. At 10 weeks of age body lean, protein and moisture percentages were lower, whereas fat percentage was higher in IGFBP-2 transgenic mice. Muscle weights were reduced (-13% at d 30; -14% at d 72), which resulted from slower growth of myofibers in size, but not from decreases in myofiber nu...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3604018</comments>
            <pubDate>Mon, 24 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3604018</guid>        </item>
        <item>
            <title>The unfolded protein response is activated in skeletal muscle by high-fat feeding: potential role in the down-regulation of protein synthesis.</title>
            <link>http://www.medworm.com/index.php?rid=3604017&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%3D20501874%26dopt%3DAbstract</link>
            <description>Authors: Deldicque L, Cani PD, Philp A, Raymackers JM, Meakin PJ, Ashford ML, Delzenne NM, Francaux M, Baar K
    High-fat diets are known to decrease muscle protein synthesis, the adaptation to overload and insulin sensitivity. Conditions that disrupt endoplasmic reticulum (ER) homeostasis lead to the activation of the unfolded protein response (UPR) that is associated with decreases in protein synthesis, chronic inflammation, and insulin resistance. The purpose of the present study was to establish whether ER stress is induced by a high-fat diet in skeletal muscle and whether ER stress can decrease mTORC1 activity and protein synthesis in muscle cells. Two independent protocols of high-fat feeding activated the UPR in mice. In the first study, mice consuming a high-fat diet containing 70...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3604017</comments>
            <pubDate>Mon, 24 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3604017</guid>        </item>
        <item>
            <title>Measuring GLUT4 translocation in mature muscle fibers.</title>
            <link>http://www.medworm.com/index.php?rid=3604016&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%3D20501875%26dopt%3DAbstract</link>
            <description>The objective of this review is to highlight how advances in recent experimental approaches translate into an enhanced understanding of the regulation of GLUT4 translocation and glucose transport in mature skeletal muscle.
    PMID: 20501875 [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=3604016</comments>
            <pubDate>Mon, 24 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3604016</guid>        </item>
        <item>
            <title>Nootkatone, a characteristic constituent of grapefruit, stimulates energy metabolism and prevents diet-induced obesity by activating AMPK.</title>
            <link>http://www.medworm.com/index.php?rid=3604015&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%3D20501876%26dopt%3DAbstract</link>
            <description>Authors: Murase T, Misawa K, Haramizu S, Minegishi Y, Hase T
    AMP-activated protein kinase (AMPK) is a serine/threonine kinase that is implicated in the control of energy metabolism, and is considered to be a molecular target for the suppression of obesity and the treatment of metabolic syndrome. Here, we identified and characterized nootkatone, a constituent of grapefruit, as a naturally occurring AMPK activator. Nootkatone induced an increase in AMPKalpha1 and alpha2 activity along with an increase in the AMP/ATP ratio and an increase the phosphorylation of AMPKalpha and the downstream target, acetyl-CoA carboxylase (ACC), in C2C12 cells. Nootkatone-induced activation of AMPK was possibly mediated both by LKB1 and CaMKK. Nootkatone also upregulated PGC-1alpha in C2C12 cells and C57BL/...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3604015</comments>
            <pubDate>Mon, 24 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3604015</guid>        </item>
        <item>
            <title>AGE, SEX AND LACTATING STATUS REGULATE GHRELIN SECRETION AND GOAT mRNA LEVELS FROM ISOLATED STOMACH.</title>
            <link>http://www.medworm.com/index.php?rid=3604014&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%3D20501877%26dopt%3DAbstract</link>
            <description>In conclusion, the stomach itself regulates ghrelin and GOAT production in order to adapt the organism to the metabolic requirements demanded through each stage of life.
    PMID: 20501877 [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=3604014</comments>
            <pubDate>Mon, 24 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3604014</guid>        </item>
        <item>
            <title>Sodium bicarbonate ingestion prior to training improves mitochondrial adaptations in rats.</title>
            <link>http://www.medworm.com/index.php?rid=3586515&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%3D20484007%26dopt%3DAbstract</link>
            <description>Authors: Bishop DJ, Thomas C, Moore-Morris T, Tonkonogi M, Sahlin K, Mercier J
    We tested the hypothesis that reducing hydrogen ion accumulation during training would result in greater improvements in muscle oxidative capacity and time to exhaustion (TTE). Male Wistar rats were randomly assigned to one of three groups (CON, PLA, BIC). CON served as a sedentary control, while PLA ingested water and BIC ingested sodium bicarbonate 30 min prior to every training session. Training consisted of 7 - 12, 2-min intervals performed 5x/wk for 5 wk. Following training, TTE was significantly greater in BIC (81.2 +/- 24.7 min) compared to PLA (53.5 +/- 30.4 min), and TTE for both groups was greater than CON (6.5 +/- 2.5 min). Fibre respiration was determined in the soleus (SOL) and extensor digitoru...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3586515</comments>
            <pubDate>Mon, 17 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3586515</guid>        </item>
        <item>
            <title>Roles for mirna-378/378* in adipocyte gene expression and lipogenesis.</title>
            <link>http://www.medworm.com/index.php?rid=3586514&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%3D20484008%26dopt%3DAbstract</link>
            <description>In this study, we explored the roles of microRNAs in adipocyte differentiation and metabolism. We first knocked-down Argonaute2 (Ago2), a key enzyme in the processing of microRNAs, to investigate a potential role for microRNAs in adipocyte differentiation and/or metabolism. Whereas we did not observe dramatic differences in adipogenesis between Ago2 knock-down and control 3T3-L1 cells, incorporation of (14)C glucose or acetate into triacylglycerol, and steady state levels of triacyglycerol, were all reduced, suggesting a role for microRNAs in adipocyte metabolism. To study roles of specific miRNAs in adipocyte biology, we screened for miRNAs that are differentially expressed between preadipocytes and adipocytes for the 3T3-L1 and ST2 cell lines. Distinct subsets of miRNAs decline or increa...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3586514</comments>
            <pubDate>Mon, 17 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3586514</guid>        </item>
        <item>
            <title>Ectopic Expression of eIF2B{varepsilon} in Rat Skeletal Muscle Rescues the Sepsis-Induced Reduction in Guanine Nucleotide Exchange Activity and Protein Synthesis.</title>
            <link>http://www.medworm.com/index.php?rid=3586513&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%3D20484009%26dopt%3DAbstract</link>
            <description>The objective of the study described here was to directly examine the effects of exogenously expressed eIF2Bepsilon in vivo on GEF activity and protein synthetic rates in rat skeletal muscle. A plasmid encoding FLAG-eIF2Bepsilon was transfected into the tibialis anterior (TA) of one leg while the contralateral TA received a control plasmid. Ectopic expression of eIF2Bepsilon resulted in increased GEF activity in TA homogenates of healthy rats demonstrating that the expressed protein was catalytically active. In an effort to restore a deficit in eIF2B activity, we utilized an established model of chronic sepsis in which skeletal muscle eIF2B activity is known to be impaired. Ectopic expression of eIF2Bepsilon in the TA rescued the sepsis-induced deficit in GEF activity and muscle protein sy...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3586513</comments>
            <pubDate>Mon, 17 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3586513</guid>        </item>
        <item>
            <title>Systemic inflammation activates the nuclear factor-{kappa}B regulatory pathway in adipose tissue.</title>
            <link>http://www.medworm.com/index.php?rid=3586512&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%3D20484010%26dopt%3DAbstract</link>
            <description>In conclusion, we present the novel finding that this model of inflammation induced a strong inflammatory response in both omental and subcutaneous AT including adhesion of macrophages to an activated endothelium and release of IL-6 from AT interstitium. It can be hypothesized that AT exerts a modulatory effect on innate immunity in humans.
    PMID: 20484010 [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=3586512</comments>
            <pubDate>Mon, 17 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3586512</guid>        </item>
        <item>
            <title>Cafeteria-diet induced insulin resistance is not associated with decreased insulin signaling or AMPK activity and is alleviated by physical training in rats.</title>
            <link>http://www.medworm.com/index.php?rid=3586511&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%3D20484011%26dopt%3DAbstract</link>
            <description>In conclusion, surplus energy intake of a palatable but low fat cafeteria diet resulted in obesity and insulin resistance which was rescued by exercise training. Interestingly, insulin resistance was not accompanied by major defects in the insulin signalling cascade or in altered AMPK expression or phosphorylation. Thus compared to previous studies of high fat feeding where insulin signalling is significantly impaired the mechanism by which CAF diet induces insulin resistance seems different.
    PMID: 20484011 [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=3586511</comments>
            <pubDate>Mon, 17 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3586511</guid>        </item>
        <item>
            <title>Lipid mobilization in subcutaneous adipose tissue during exercise in lean and obese humans. the roles of insulin and natriuretic peptides.</title>
            <link>http://www.medworm.com/index.php?rid=3586510&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%3D20484012%26dopt%3DAbstract</link>
            <description>LIPID MOBILIZATION IN SUBCUTANEOUS ADIPOSE TISSUE DURING EXERCISE IN LEAN AND OBESE HUMANS. THE ROLES OF INSULIN AND NATRIURETIC PEPTIDES.
    Am J Physiol Endocrinol Metab. 2010 May 18;
    Authors: Koppo K, Larrouy D, Marques MA, Berlan M, Bajzova M, Polak J, Van De Voorde J, Bulow J, Lafontan M, Crampes F, Langin D, Stich V, de Glisezinski I
    The aim of this study was to evaluate the relative contribution of various hormones involved in the regulation of lipid mobilization in subcutaneous adipose tissue (SCAT) during exercise and to assess the impact of obesity on this regulation. Eight lean and eight obese men performed a 60 min cycle exercise bout at 50% of their peak oxygen uptake on two occasions: during intravenous infusion of physiological saline (control condition) or octreoti...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3586510</comments>
            <pubDate>Mon, 17 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3586510</guid>        </item>
        <item>
            <title>Adipose differentiation-related protein regulates lipids and insulin in pancreatic islet.</title>
            <link>http://www.medworm.com/index.php?rid=3586509&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%3D20484013%26dopt%3DAbstract</link>
            <description>Authors: Faleck D, Ali K, Roat R, Graham MJ, Crooke RM, Battisti R, Garcia E, Ahima RS, Imai Y
    The excess accumulation of lipids in islets is thought to contribute to the development of diabetes in obesity by impairing beta cell function. However, lipids also serve a nutrient function in islets, and fatty acids acutely increase insulin secretion. A better understanding of lipid metabolism in islets will shed light on complex effects of lipids on beta cells. Adipose differentiation-related protein (ADFP) is localized on the surface of lipid droplets in a wide range of cells and plays an important role in intracellular lipid metabolism. We found that ADFP was highly expressed in murine beta cells. Moreover, islet ADFP was increased in mice on a high-fat diet (3.5 fold of control) and aft...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3586509</comments>
            <pubDate>Mon, 17 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3586509</guid>        </item>
        <item>
            <title>Exercise training increases sarcolemmal and mitochondrial fatty acid transport proteins in human skeletal muscle.</title>
            <link>http://www.medworm.com/index.php?rid=3586508&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%3D20484014%26dopt%3DAbstract</link>
            <description>EXERCISE TRAINING INCREASES SARCOLEMMAL AND MITOCHONDRIAL FATTY ACID TRANSPORT PROTEINS IN HUMAN SKELETAL MUSCLE.
    Am J Physiol Endocrinol Metab. 2010 May 18;
    Authors: Talanian JL, Holloway GP, Snook LA, Heigenhauser GJ, Bonen A, Spriet LL
    Fatty acid oxidation is highly regulated in skeletal muscle, with several sites of regulation, including the transport of fatty acids across the plasma and mitochondrial membranes. Transport across these membranes is primarily protein mediated, limited by the abundance of fatty acid transport proteins on the respective membranes. Recent evidence has shown that fatty acid transport proteins move in response to acute and chronic perturbations, however in human skeletal muscle the localization of fatty acid transport proteins in response to train...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3586508</comments>
            <pubDate>Mon, 17 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3586508</guid>        </item>
        <item>
            <title>The Obese Carboxypeptidase E Knockout Mouse Exhibit Multiple Defects in Peptide Hormone Processing Contributing to Low Bone Mineral Density.</title>
            <link>http://www.medworm.com/index.php?rid=3557392&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%3D20460579%26dopt%3DAbstract</link>
            <description>This study highlights the complex physiological interplay between peptides involved in energy metabolism and bone formation and furthermore suggests the possibility that patients, bearing CPE and CART mutations leading to inactive forms of these molecules, may be at a higher risk of developing osteoporosis.
    PMID: 20460579 [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=3557392</comments>
            <pubDate>Mon, 10 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3557392</guid>        </item>
        <item>
            <title>Methylglyoxal Increases Cardiomyocyte Ischemia/Reperfusion Injury via Glycative Inhibition of Thioredoxin Activity.</title>
            <link>http://www.medworm.com/index.php?rid=3557391&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%3D20460580%26dopt%3DAbstract</link>
            <description>Authors: Wang XL, Lau WB, Yuan YX, Wang YJ, Yi W, Christopher TA, Lopez BL, Liu HR, Ma XL
    Diabetes (DM) is closely related to cardiovascular morbidity and mortality, but the specific molecular basis linking DM with increased vulnerability to cardiovascular injury remains incompletely understood. Methylglyoxal (MG), a precursor to advanced glycation end-products (AGEs), is increased in diabetic patient plasma but its role in diabetic cardiovascular complications is unclear. Thioredoxin (Trx), a cytoprotective molecule with anti-apoptotic function, has been demonstrated to be vulnerable to glycative inhibition, but whether Trx is glycatively inhibited by MG thus contributing to increased cardiac injury has never been investigated. Cultured H9c2 cardiomyocytes were treated with MG (200mic...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3557391</comments>
            <pubDate>Mon, 10 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3557391</guid>        </item>
        <item>
            <title>Am J Physiol Endocrinol Metab; +20 new citations</title>
            <link>http://www.medworm.com/index.php?rid=3534612&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%25222010%252F04%252F30%252005.44%2522%255BMHDA%255D%253A%25222010%252F05%252F05%252020.18%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%25222010%252F04%252F30%252005.44%2522%255BEDAT%255D%29%29</link>
            <description>20 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 2010/05/05PubMed, 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=3534612</comments>
            <pubDate>Thu, 06 May 2010 00:18:02 +0100</pubDate>
            <guid isPermaLink="false">3534612</guid>        </item>
        <item>
            <title>Glutamine: precursor or nitrogen donor for citrulline synthesis?</title>
            <link>http://www.medworm.com/index.php?rid=3494683&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%3D20407005%26dopt%3DAbstract</link>
            <description>In conclusion, dietary glutamine is a poor carbon skeleton precursor for the synthesis of citrulline, although it contributes both nonspecific nitrogen and carbon to citrulline synthesis.
    PMID: 20407005 [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=3494683</comments>
            <pubDate>Mon, 19 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3494683</guid>        </item>
        <item>
            <title>The effect of physical training on insulin secretion and action in skeletal muscle and adipose tissue of first degree relatives to type 2 diabetic patients.</title>
            <link>http://www.medworm.com/index.php?rid=3494682&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%3D20407006%26dopt%3DAbstract</link>
            <description>Conclusions: Insulin secretory capacity is lower in FDR than CON, and there is dissociation between training-induced changes in insulin secretion and insulin-mediated glucose uptake. Maximal glucose uptake rates are similar between groups and increases with physical training.
    PMID: 20407006 [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=3494682</comments>
            <pubDate>Mon, 19 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3494682</guid>        </item>
        <item>
            <title>Acute inflammation reduces kisspeptin immunoreactivity at the arcuate nucleus and decreases responsiveness to kisspeptin independently of its anorectic effects.</title>
            <link>http://www.medworm.com/index.php?rid=3494681&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%3D20407007%26dopt%3DAbstract</link>
            <description>Authors: Castellano JM, Bentsen AH, Romero M, Pineda R, Ruiz-Pino F, Garcia-Galiano D, Sanchez-Garrido MA, Pinilla L, Mikkelsen JD, Tena-Sempere M
    Severe inflammatory challenges are frequently coupled to decreased food intake and disruption of reproductive function; the latter via deregulation of different signalling pathways which impinge onto GnRH neurons. Recently, the hypothalamic Kiss1 system, a major gatekeeper of GnRH function, has been suggested as potential target for transmitting immune-mediated repression of the gonadotropic axis during acute inflammation; yet, key facets of such phenomenon remain ill defined. Using lipopolysaccharide S (LPS)-treated male rats as model of inflammation, we document herein the pattern of hypothalamic kisspeptin immunoreactivity (IR) and hormon...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3494681</comments>
            <pubDate>Mon, 19 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3494681</guid>        </item>
        <item>
            <title>Role of N-linked glycosylation in biosynthesis, trafficking, and function of the human glucagon-like peptide 1 receptor.</title>
            <link>http://www.medworm.com/index.php?rid=3494680&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%3D20407008%26dopt%3DAbstract</link>
            <description>Authors: Chen Q, Miller LJ, Dong M
    The family B G protein-coupled glucagon-like peptide 1 (GLP1) receptor is an important drug target for treatment of type 2 diabetes. Like other family members, the GLP1 receptor is a glycosylated membrane protein that contains three potential sites for N-linked glycosylation within the functionally-important extracellular amino-terminal domain. However, the roles for each potential site of glycosylation in receptor biosynthesis, trafficking, and function are not known. In this work, we demonstrated that tunicamycin inhibition of glycosylation of the GLP1 receptor expressed in CHO cells interfered with biosynthesis and intracellular trafficking, thereby eliminating natural ligand binding. To further investigate the roles of each of the glycosylation si...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3494680</comments>
            <pubDate>Mon, 19 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3494680</guid>        </item>
        <item>
            <title>The Many Facets of PPAR{gamma}: Novel Insights for the Skeleton.</title>
            <link>http://www.medworm.com/index.php?rid=3494679&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%3D20407009%26dopt%3DAbstract</link>
            <description>Authors: Kawai M, Sousa KM, Macdougald OA, Rosen CJ
    Peroxisome proliferator-activated receptor gamma (PPARgamma) is a nuclear receptor that functions as a master transcriptional regulator of adipocyte conversion. During PPARgamma transactivation, multiple signaling pathways interact with one another, leading to the differentiation of both white and brown adipose tissue. Ligand activation of the PPARgamma-RXR heterodimer complex also enhances insulin sensitivity and this property has been heavily exploited to develop effective pharmacotherapies for the treatment of type II diabetes mellitus. PPARgamma is also expressed in stem cells and plays a critical role in mesenchymal stromal cell differentiation and lineage determination events. The many facets of PPARgamma activity within the bon...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3494679</comments>
            <pubDate>Mon, 19 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3494679</guid>        </item>
        <item>
            <title>LATS1 phosphorylates Forkhead L2 and regulates its transcriptional activity.</title>
            <link>http://www.medworm.com/index.php?rid=3494678&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%3D20407010%26dopt%3DAbstract</link>
            <description>In this study, we investigated whether FOXL2's activity as a transcriptional repressor is regulated by phosphorylation. We found that FOXL2 is phosphorylated at a serine residue and, using yeast two-hybrid screening, identified LATS1 as a potential FOXL2-interacting protein. LATS1 is a serine/threonine kinase whose deletion in mice results in an ovarian phenotype similar to POF. Using co-immunoprecipitation and kinase assays, we confirmed that LATS1 binds to FOXL2, and demonstrated that LATS1 phosphorylates FOXL2 at a serine residue. Moreover, we found that FOXL2 and LATS1 are co-expressed in developing mouse gonads and in granulosa cells of small and medium follicles in the mouse ovary. Lastly, we demonstrated that co-expression with LATS1 enhances FOXL2's activity as a repressor of the S...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3494678</comments>
            <pubDate>Mon, 19 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3494678</guid>        </item>
        <item>
            <title>Am J Physiol Endocrinol Metab; +19 new citations</title>
            <link>http://www.medworm.com/index.php?rid=3468673&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%25222010%252F04%252F09%252014.00%2522%255BMHDA%255D%253A%25222010%252F04%252F15%252005.00%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%25222010%252F04%252F09%252014.00%2522%255BEDAT%255D%29%29</link>
            <description>19 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 2010/04/15PubMed, 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=3468673</comments>
            <pubDate>Thu, 15 Apr 2010 09:00:03 +0100</pubDate>
            <guid isPermaLink="false">3468673</guid>        </item>
        <item>
            <title>Am J Physiol Endocrinol Metab; +39 new citations</title>
            <link>http://www.medworm.com/index.php?rid=3429949&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%25222010%252F03%252F25%252015.00%2522%255BMHDA%255D%253A%25222010%252F04%252F02%252002.26%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%25222010%252F03%252F25%252015.00%2522%255BEDAT%255D%29%29</link>
            <description>39 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 2010/04/02PubMed, 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=3429949</comments>
            <pubDate>Fri, 02 Apr 2010 06:26:02 +0100</pubDate>
            <guid isPermaLink="false">3429949</guid>        </item>
        <item>
            <title>Computational Model of Cellular Metabolic Dynamics: Effect of Insulin on Glucose Disposal in Human Skeletal Muscle.</title>
            <link>http://www.medworm.com/index.php?rid=3404261&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%3D20332360%26dopt%3DAbstract</link>
            <description>Authors: Li Y, Solomon TP, Haus JM, Saidel GM, Cabrera ME, Kirwan JP
    Identifying the mechanisms by which insulin regulates glucose metabolism in skeletal muscle is critical to understanding the etiology of insulin resistance and type 2 diabetes. Our knowledge of these mechanisms is limited by the difficulty of obtaining in vivo intracellular data. To quantitatively distinguish significant transport and metabolic mechanisms from limited experimental data, we developed a physiologically based, multi-scale mathematical model of cellular metabolic dynamics in skeletal muscle. The model describes mass transport and metabolic processes including distinctive processes of the cytosol and mitochondria. The model simulated skeletal muscle metabolic responses to insulin corresponding to human hyp...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3404261</comments>
            <pubDate>Tue, 23 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3404261</guid>        </item>
        <item>
            <title>Systemic activation of glutamate dehydrogenase increases renal ammoniagenesis: implications for the hyperinsulinism/hyperammonemia syndrome.</title>
            <link>http://www.medworm.com/index.php?rid=3404260&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%3D20332361%26dopt%3DAbstract</link>
            <description>We examined the effect of systemic activation of GDH on ammonia metabolism in the rat. 2-aminobicyclo (2.2.1) heptane 2-carboxylic acid (BCH) is a non-metabolizable analogue of the natural GDH allosteric activator leucine. A dose of 100 micromol BCH * 100 g(-1) rat resulted in a mild systemic hyperammonemia. Using arterial-venous (A-V) differences, we exclude the liver, intestine and skeletal muscle as major contributors to this BCH induced hyperammonemia. However, renal ammonia output increased as demonstrated by an increase in A-V difference for ammonia across the kidney in BCH-treated animals. Isolated renal cortical tubules incubated with BCH increased the rate of ammoniagenesis from glutamine by 40%. The flux through GDH increased over 2-fold when BCH was added to renal mitochondria r...</description>
            <author>Am J Physiol Endocri...</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3404260</comments>
            <pubDate>Tue, 23 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3404260</guid>        </item>
        <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>
    </channel>
</rss>

