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        <title>Diabetes 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 'Diabetes' source.</description>
        <link><![CDATA[http://www.medworm.com/rss/search.php?qu=Diabetes&t=Diabetes&s=Search&f=source]]></link>
        <lastBuildDate>Wed, 08 Feb 2012 15:08:52 +0100</lastBuildDate>
        <item>
            <title>Damaging Loss of Self-Control by Stressed β-Cells.</title>
            <link>http://www.medworm.com/index.php?rid=5663176&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22275082%26dopt%3DAbstract</link>
            <description>Authors: Holness MJ, Sugden MC
    PMID: 22275082 [PubMed - in process] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5663176</comments>
            <pubDate>Wed, 01 Feb 2012 05:00:00 +0100</pubDate>
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        <item>
            <title>Prediabetes: Evaluation of β-Cell Function.</title>
            <link>http://www.medworm.com/index.php?rid=5663175&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22275083%26dopt%3DAbstract</link>
            <description>Authors: Basu A, Pedersen MG, Cobelli C
    PMID: 22275083 [PubMed - in process] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5663175</comments>
            <pubDate>Wed, 01 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5663175</guid>        </item>
        <item>
            <title>Mapping autophagy on to your metabolic radar.</title>
            <link>http://www.medworm.com/index.php?rid=5663174&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22275084%26dopt%3DAbstract</link>
            <description>Authors: Yamada E, Singh R
    PMID: 22275084 [PubMed - in process] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5663174</comments>
            <pubDate>Wed, 01 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5663174</guid>        </item>
        <item>
            <title>Insulin augmentation of glucose-stimulated insulin secretion is impaired in insulin-resistant humans.</title>
            <link>http://www.medworm.com/index.php?rid=5663173&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22275085%26dopt%3DAbstract</link>
            <description>Authors: Halperin F, Lopez X, Manning R, Kahn CR, Kulkarni RN, Goldfine AB
    Abstract
    Type 2 diabetes (T2D) is characterized by insulin resistance and pancreatic β-cell dysfunction, the latter possibly caused by a defect in insulin signaling in β-cells. We hypothesized that insulin's effect to potentiate glucose-stimulated insulin secretion (GSIS) would be diminished in insulin-resistant persons. To evaluate the effect of insulin to modulate GSIS in insulin-resistant compared with insulin-sensitive subjects, 10 participants with impaired glucose tolerance (IGT), 11 with T2D, and 8 healthy control subjects were studied on two occasions. The insulin secretory response was assessed by the administration of dextrose for 80 min following a 4-h clamp with either saline infusion (sham) or...</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5663173</comments>
            <pubDate>Wed, 01 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5663173</guid>        </item>
        <item>
            <title>Distinct β-Cell Defects in Impaired Fasting Glucose and Impaired Glucose Tolerance.</title>
            <link>http://www.medworm.com/index.php?rid=5663172&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22275086%26dopt%3DAbstract</link>
            <description>Authors: Kanat M, Mari A, Norton L, Winnier D, Defronzo RA, Jenkinson C, Abdul-Ghani MA
    Abstract
    To characterize the defects in β-cell function in subjects with impaired fasting glucose (IFG) and compare the results to impaired glucose tolerance (IGT) and normal glucose tolerance (NGT) subjects, β-cell glucose sensitivity and rate sensitivity during the oral glucose tolerance test were measured with the model by Mari in 172 Mexican Americans. A subgroup (n = 70) received a 2-h hyperglycemic clamp (+125 mg/dL), and first- and second-phase insulin secretion were quantitated. Compared with NGT, subjects with IFG and IGT manifested a decrease in β-cell glucose sensitivity; IFG subjects, but not IGT subjects, had decreased β-cell rate sensitivity. In IFG subjects, the defect in β-c...</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5663172</comments>
            <pubDate>Wed, 01 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5663172</guid>        </item>
        <item>
            <title>Issues and events.</title>
            <link>http://www.medworm.com/index.php?rid=5663171&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22275088%26dopt%3DAbstract</link>
            <description>Authors: 
    PMID: 22275088 [PubMed - in process] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5663171</comments>
            <pubDate>Wed, 01 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5663171</guid>        </item>
        <item>
            <title>Chronic GLP-1 Receptor Activation by Exendin-4 Induces Expansion of Pancreatic Duct Glands in Rats and Accelerates Formation of Dysplastic Lesions and Chronic Pancreatitis in the KrasG12D Mouse Model.</title>
            <link>http://www.medworm.com/index.php?rid=5626202&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22266668%26dopt%3DAbstract</link>
            <description>Authors: Gier B, Matveyenko AV, Kirakossian D, Dawson D, Dry SM, Butler PC
    Abstract
    Pancreatic duct glands (PDGs) have been hypothesized to give rise to pancreatic intraepithelial neoplasia (PanIN). Treatment with the glucagon-like peptide (GLP)-1 analog, exendin-4, for 12 weeks induced the expansion of PDGs with mucinous metaplasia and columnar cell atypia resembling low-grade PanIN in rats. In the pancreata of Pdx1-Cre; LSL-Kras(G12D) mice, exendin-4 led to acceleration of the disruption of exocrine architecture and chronic pancreatitis with mucinous metaplasia and increased formation of murine PanIN lesions. PDGs and PanIN lesions in rodent and human pancreata express the GLP-1 receptor. Exendin-4 induced proproliferative signaling pathways in human pancreatic duct cells, cAMP-p...</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5626202</comments>
            <pubDate>Fri, 20 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5626202</guid>        </item>
        <item>
            <title>Peroxisome Proliferator-Activated Receptor-γ Coactivator-1α (PGC-1α) Enhances Engraftment and Angiogenesis of Mesenchymal Stem Cells in Diabetic Hindlimb Ischemia.</title>
            <link>http://www.medworm.com/index.php?rid=5626201&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22266669%26dopt%3DAbstract</link>
            <description>Authors: Lu D, Zhang L, Wang H, Zhang Y, Liu J, Xu J, Liang Z, Deng W, Jiang Y, Wu Q, Li S, Ai Z, Zhong Y, Ying Y, Liu H, Gao F, Zhang Z, Chen B
    Abstract
    To examine whether the peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α), a key regulator linking angiogenesis and metabolism, could enhance the engraftment and angiogenesis of mesenchymal stem cells (MSCs) in diabetic hindlimb ischemia, we engineered the overexpression of PGC-1α within MSCs using an adenoviral vector encoding green fluorescent protein and PGC-1α, and then tested the survivability and angiogenesis of MSCs in vitro and in vivo. Under the condition of hypoxia concomitant with serum deprivation, the overexpression of PGC-1α in MSCs resulted in a higher expression level of hypoxia-inducible fa...</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5626201</comments>
            <pubDate>Fri, 20 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5626201</guid>        </item>
        <item>
            <title>A Genome-Wide Association Study of Gestational Diabetes Mellitus in Korean Women.</title>
            <link>http://www.medworm.com/index.php?rid=5580102&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22233651%26dopt%3DAbstract</link>
            <description>In conclusion, we have confirmed that genetic variants in CDKAL1 and near MTNR1B are strongly associated with GDM in Korean women. There seems to be a shared genetic basis between GDM and type 2 diabetes.
    PMID: 22233651 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5580102</comments>
            <pubDate>Tue, 10 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5580102</guid>        </item>
        <item>
            <title>Heritable Transmission of Diabetic Metabolic Memory in Zebrafish Correlates With DNA Hypomethylation and Aberrant Gene Expression.</title>
            <link>http://www.medworm.com/index.php?rid=5580109&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22228713%26dopt%3DAbstract</link>
            <description>Authors: Olsen AS, Sarras MP, Leontovich A, Intine RV
    Abstract
    Metabolic memory (MM) is the phenomenon whereby diabetes complications persist and progress after glycemic recovery is achieved. Here, we present data showing that MM is heritable and that the transmission correlates with hyperglycemia-induced DNA hypomethylation and aberrant gene expression. Streptozocin was used to induce hyperglycemia in adult zebrafish, and then, following streptozocin withdrawal, a recovery phase was allowed to reestablish a euglycemic state. Blood glucose and serum insulin returned to physiological levels during the first 2 weeks of the recovery phase as a result of pancreatic β-cell regeneration. In contrast, caudal fin regeneration and skin wound healing remained impaired to the same extent as ...</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5580109</comments>
            <pubDate>Fri, 06 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5580109</guid>        </item>
        <item>
            <title>CGI-58/ABHD5-Derived Signaling Lipids Regulate Systemic Inflammation and Insulin Action.</title>
            <link>http://www.medworm.com/index.php?rid=5580108&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22228714%26dopt%3DAbstract</link>
            <description>Authors: Lord CC, Betters JL, Ivanova PT, Milne SB, Myers DS, Madenspacher J, Thomas G, Chung S, Liu M, Davis MA, Lee RG, Crooke RM, Graham MJ, Parks JS, Brasaemle DL, Fessler MB, Brown HA, Brown JM
    Abstract
    Mutations of comparative gene identification 58 (CGI-58) in humans cause Chanarin-Dorfman syndrome, a rare autosomal recessive disease in which excess triacylglycerol (TAG) accumulates in multiple tissues. CGI-58 recently has been ascribed two distinct biochemical activities, including coactivation of adipose triglyceride lipase and acylation of lysophosphatidic acid (LPA). It is noteworthy that both the substrate (LPA) and the product (phosphatidic acid) of the LPA acyltransferase reaction are well-known signaling lipids. Therefore, we hypothesized that CGI-58 is involved in g...</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5580108</comments>
            <pubDate>Fri, 06 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5580108</guid>        </item>
        <item>
            <title>Storage Rates of Circulating Free Fatty Acid Into Adipose Tissue During Eating or Walking in Humans.</title>
            <link>http://www.medworm.com/index.php?rid=5580107&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22228715%26dopt%3DAbstract</link>
            <description>Authors: Koutsari C, Mundi MS, Ali AH, Jensen MD
    Abstract
    We measured subcutaneous adipose tissue free fatty acid (FFA) storage rates in postprandial and walking conditions to better understand the contributions of this pathway to body fat distribution. Palmitate tracers were infused intravenously and fat biopsies collected to measure palmitate storage in upper- (UBSQ) and lower-body subcutaneous (LBSQ) fat in 41 (17 men) and 40 (16 men) volunteers under postprandial and under postabsorptive walking conditions, respectively. Postprandial palmitate storage was greater in women than men in UBSQ (0.50 ± 0.25 vs. 0.33 ± 0.37 μmol ⋅ kg fat(-1) ⋅ min(-1); P = 0.007) and LBSQ fat (0.37 ± 0.25 vs. 0.22 ± 0.20 μmol ⋅ kg fat(-1) ⋅ min(-1); P = 0.005); storage rates were signifi...</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5580107</comments>
            <pubDate>Fri, 06 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5580107</guid>        </item>
        <item>
            <title>Morbid Obese Human Subjects Have Increased Peripheral Blood CD4+ T Cells With Skewing Toward a Treg- and Th2-Dominated Phenotype.</title>
            <link>http://www.medworm.com/index.php?rid=5580106&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22228716%26dopt%3DAbstract</link>
            <description>In this study, we investigated the peripheral blood T-cell compartment of morbid obese and lean subjects. We determined all major T-cell subpopulations via six-color flow cytometry, including CD8(+) and CD4(+) T cells, CD4(+) T-helper (Th) subpopulations, and natural CD4(+)CD25(+)FoxP3(+) T-regulatory (Treg) cells. Moreover, molecular analyses to assess thymic output, T-cell proliferation (T-cell receptor excision circle analysis), and T-cell receptor-β (TCRB) repertoire (GeneScan analysis) were performed. In addition, we determined plasma levels of proinflammatory cytokines and cytokines associated with Th subpopulations and T-cell proliferation. Morbid obese subjects had a selective increase in peripheral blood CD4(+) naive, memory, natural CD4(+)CD25(+)FoxP3(+) Treg, and Th2 T cells, w...</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5580106</comments>
            <pubDate>Fri, 06 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5580106</guid>        </item>
        <item>
            <title>TIMP3 Overexpression in Macrophages Protects From Insulin Resistance, Adipose Inflammation, and Nonalcoholic Fatty Liver Disease in Mice.</title>
            <link>http://www.medworm.com/index.php?rid=5580105&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22228717%26dopt%3DAbstract</link>
            <description>Authors: Menghini R, Casagrande V, Menini S, Marino A, Marzano V, Hribal ML, Gentileschi P, Lauro D, Schillaci O, Pugliese G, Sbraccia P, Urbani A, Lauro R, Federici M
    Abstract
    The tissue inhibitor of metalloproteinase (TIMP)3, a stromal protein that restrains the activity of proteases and receptors, is reduced in inflammatory metabolic disorders such as type 2 diabetes mellitus (T2DM) and atherosclerosis. We overexpressed Timp3 in mouse macrophages (MacT3) to analyze its potential antidiabetes and antiatherosclerotic effects. Transgenic mice with myeloid cells targeting overexpression of TIMP3 were generated and fed a high-fat diet for 20 weeks. Physical and metabolic phenotypes were determined. Inflammatory markers, lipid accumulation, and insulin sensitivity were measured in whi...</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5580105</comments>
            <pubDate>Fri, 06 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5580105</guid>        </item>
        <item>
            <title>Activation of Endoplasmic Reticulum Stress by Hyperglycemia Is Essential for Muller Cell-Derived Inflammatory Cytokine Production in Diabetes.</title>
            <link>http://www.medworm.com/index.php?rid=5580104&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22228718%26dopt%3DAbstract</link>
            <description>Authors: Zhong Y, Li J, Chen Y, Wang JJ, Ratan R, Zhang SX
    Abstract
    Inflammation plays an important role in diabetes-induced retinal vascular leakage. The purpose of this study is to examine the role of endoplasmic reticulum (ER) stress and the signaling pathway of ER stress-induced activating transcription factor 4 (ATF4) in the regulation of Müller cell-derived inflammatory mediators in diabetic retinopathy. In diabetic animals, elevated ER stress markers, ATF4, and vascular endothelial growth factor (VEGF) expression were partially localized to Müller cells in the retina. In cultured Müller cells, high glucose induced a time-dependent increase of ER stress, ATF4 expression, and inflammatory factor production. Inducing ER stress or overexpressing ATF4 resulted in elevated intr...</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5580104</comments>
            <pubDate>Fri, 06 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5580104</guid>        </item>
        <item>
            <title>Common Variants of IL6, LEPR, and PBEF1 Are Associated With Obesity in Indian Children.</title>
            <link>http://www.medworm.com/index.php?rid=5580103&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22228719%26dopt%3DAbstract</link>
            <description>In conclusion, our results demonstrate the association of the common variants of IL6, LEPR, and PBEF1 with obesity in Indian children.
    PMID: 22228719 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5580103</comments>
            <pubDate>Fri, 06 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5580103</guid>        </item>
        <item>
            <title>Hyperglycemia Enhances IGF-I-Stimulated Src Activation via Increasing Nox4-Derived Reactive Oxygen Species in a PKCζ-Dependent Manner in Vascular Smooth Muscle Cells.</title>
            <link>http://www.medworm.com/index.php?rid=5538101&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22148072%26dopt%3DAbstract</link>
            <description>Authors: Xi G, Shen X, Maile LA, Wai C, Gollahon K, Clemmons DR
    Abstract
    IGF-I-stimulated sarcoma viral oncogene (Src) activation during hyperglycemia is required for propagating downstream signaling. The aim of the current study was to determine the mechanism by which hyperglycemia enhances IGF-I-stimulated Src activation and the role of NADPH oxidase 4 (Nox4) and protein kinase C ζ (PKCζ) in mediating this response in vascular smooth muscle cells (VSMCs). Nox4 expression was analyzed in VSMCs exposed to hyperglycemia. The role of Nox4-derived reactive oxygen species (ROS) in IGF-I-stimulated Src activation was investigated via knockdown of Nox4. Different isoforms of PKC were screened to investigate their role in hyperglycemia-induced Nox4. The oxidation of Src was shown to be ...</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538101</comments>
            <pubDate>Sun, 25 Dec 2011 06:10:02 +0100</pubDate>
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        <item>
            <title>Changing of the guards.</title>
            <link>http://www.medworm.com/index.php?rid=5538098&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22187368%26dopt%3DAbstract</link>
            <description>Authors: Nair KS
    PMID: 22187368 [PubMed - in process] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538098</comments>
            <pubDate>Sun, 25 Dec 2011 06:09:31 +0100</pubDate>
            <guid isPermaLink="false">5538098</guid>        </item>
        <item>
            <title>Banting lecture 2011: hyperinsulinemia: cause or consequence?</title>
            <link>http://www.medworm.com/index.php?rid=5538097&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22187369%26dopt%3DAbstract</link>
            <description>Authors: Corkey BE
    Abstract
    The Banting Medal for Scientific Achievement Award is the American Diabetes Association's highest scientific award and honors an individual who has made significant, long-term contributions to the understanding of diabetes, its treatment, and/or prevention. The award is named after Nobel Prize winner Sir Frederick Banting, who codiscovered insulin treatment for diabetes. Dr. Barbara E. Corkey received the American Diabetes Association's Banting Medal for Scientific Achievement at the Association's 71st Scientific Sessions, 24-28 June 2011, San Diego, California. She presented the Banting Lecture, &quot;Hyperinsulinemia: Cause or Consequence?&quot; on Sunday, 26 June 2011.
    PMID: 22187369 [PubMed - in process] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538097</comments>
            <pubDate>Sun, 25 Dec 2011 06:09:21 +0100</pubDate>
            <guid isPermaLink="false">5538097</guid>        </item>
        <item>
            <title>Central role for interleukin-2 in type 1 diabetes.</title>
            <link>http://www.medworm.com/index.php?rid=5538096&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22187370%26dopt%3DAbstract</link>
            <description>Authors: Hulme MA, Wasserfall CH, Atkinson MA, Brusko TM
    Abstract
    Type 1 diabetes presents clinically with overt hyperglycemia resulting from progressive immune-mediated destruction of pancreatic β-cells and associated metabolic dysfunction. Combined genetic and immunological studies now highlight deficiencies in both the interleukin-2 (IL-2) receptor and its downstream signaling pathway as a central defect in the pathogenesis of type 1 diabetes. Prior intervention studies in animal models indicate that augmenting IL-2 signaling can prevent and reverse disease, with protection conferred primarily by restoration of regulatory T-cell (Treg) function. In this article, we will focus on studies of type 1 diabetes noting deficient IL-2 signaling and build what we believe forms the molec...</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538096</comments>
            <pubDate>Sun, 25 Dec 2011 06:09:11 +0100</pubDate>
            <guid isPermaLink="false">5538096</guid>        </item>
        <item>
            <title>Nutrient sensing, autophagy, and diabetic nephropathy.</title>
            <link>http://www.medworm.com/index.php?rid=5538095&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22187371%26dopt%3DAbstract</link>
            <description>Authors: Kume S, Thomas MC, Koya D
    PMID: 22187371 [PubMed - in process] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538095</comments>
            <pubDate>Sun, 25 Dec 2011 06:09:01 +0100</pubDate>
            <guid isPermaLink="false">5538095</guid>        </item>
        <item>
            <title>Juvenile diabetes research foundation: mission, strategy, and priorities.</title>
            <link>http://www.medworm.com/index.php?rid=5538094&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22187372%26dopt%3DAbstract</link>
            <description>Authors: Insel RA, Deecher DC, Brewer J
    PMID: 22187372 [PubMed - in process] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538094</comments>
            <pubDate>Sun, 25 Dec 2011 06:08:50 +0100</pubDate>
            <guid isPermaLink="false">5538094</guid>        </item>
        <item>
            <title>Why are C-section deliveries linked to childhood type 1 diabetes?</title>
            <link>http://www.medworm.com/index.php?rid=5538093&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22187373%26dopt%3DAbstract</link>
            <description>Authors: Vehik K, Dabelea D
    PMID: 22187373 [PubMed - in process] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538093</comments>
            <pubDate>Sun, 25 Dec 2011 06:08:39 +0100</pubDate>
            <guid isPermaLink="false">5538093</guid>        </item>
        <item>
            <title>Updates to Policies and Procedures Related to Potential Scientific and Academic Misconduct in the Journals of the American Diabetes Association.</title>
            <link>http://www.medworm.com/index.php?rid=5538092&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22187374%26dopt%3DAbstract</link>
            <description>Authors: Kohler CS, 
    PMID: 22187374 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538092</comments>
            <pubDate>Sun, 25 Dec 2011 06:08:29 +0100</pubDate>
            <guid isPermaLink="false">5538092</guid>        </item>
        <item>
            <title>Remodeling of hepatic metabolism and hyperaminoacidemia in mice deficient in proglucagon-derived peptides.</title>
            <link>http://www.medworm.com/index.php?rid=5538091&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22187375%26dopt%3DAbstract</link>
            <description>Authors: Watanabe C, Seino Y, Miyahira H, Yamamoto M, Fukami A, Ozaki N, Takagishi Y, Sato J, Fukuwatari T, Shibata K, Oiso Y, Murata Y, Hayashi Y
    Abstract
    Glucagon is believed to be one of the most important peptides for upregulating blood glucose levels. However, homozygous glucagon-green fluorescent protein (gfp) knock-in mice (Gcg(gfp/gfp): GCGKO) are normoglycemic despite the absence of proglucagon-derived peptides, including glucagon. To characterize metabolism in the GCGKO mice, we analyzed gene expression and metabolome in the liver. The expression of genes encoding rate-limiting enzymes for gluconeogenesis was only marginally altered. On the other hand, genes encoding enzymes involved in conversion of amino acids to metabolites available for the tricarboxylic acid cycle an...</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538091</comments>
            <pubDate>Sun, 25 Dec 2011 06:08:18 +0100</pubDate>
            <guid isPermaLink="false">5538091</guid>        </item>
        <item>
            <title>Hypothalamic leucine metabolism regulates liver glucose production.</title>
            <link>http://www.medworm.com/index.php?rid=5538090&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22187376%26dopt%3DAbstract</link>
            <description>Authors: Su Y, Lam TK, He W, Pocai A, Bryan J, Aguilar-Bryan L, Gutiérrez-Juárez R
    Abstract
    Amino acids profoundly affect insulin action and glucose metabolism in mammals. Here, we investigated the role of the mediobasal hypothalamus (MBH), a key center involved in nutrient-dependent metabolic regulation. Specifically, we tested the novel hypothesis that the metabolism of leucine within the MBH couples the central sensing of leucine with the control of glucose production by the liver. We performed either central (MBH) or systemic infusions of leucine in Sprague-Dawley male rats during basal pancreatic insulin clamps in combination with various pharmacological and molecular interventions designed to modulate leucine metabolism in the MBH. We also examined the role of hypothalamic ...</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538090</comments>
            <pubDate>Sun, 25 Dec 2011 06:08:07 +0100</pubDate>
            <guid isPermaLink="false">5538090</guid>        </item>
        <item>
            <title>Targeted Loss of GHR Signaling in Mouse Skeletal Muscle Protects Against High-Fat Diet-Induced Metabolic Deterioration.</title>
            <link>http://www.medworm.com/index.php?rid=5538089&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22187377%26dopt%3DAbstract</link>
            <description>Authors: Vijayakumar A, Wu Y, Sun H, Li X, Jeddy Z, Liu C, Schwartz GJ, Yakar S, Leroith D
    Abstract
    Growth hormone (GH) exerts diverse tissue-specific metabolic effects that are not revealed by global alteration of GH action. To study the direct metabolic effects of GH in the muscle, we specifically inactivated the growth hormone receptor (ghr) gene in postnatal mouse skeletal muscle using the Cre/loxP system (mGHRKO model). The metabolic state of the mGHRKO mice was characterized under lean and obese states. High-fat diet feeding in the mGHRKO mice was associated with reduced adiposity, improved insulin sensitivity, lower systemic inflammation, decreased muscle and hepatic triglyceride content, and greater energy expenditure compared with control mice. The obese mGHRKO mice also h...</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538089</comments>
            <pubDate>Sun, 25 Dec 2011 06:07:56 +0100</pubDate>
            <guid isPermaLink="false">5538089</guid>        </item>
        <item>
            <title>Identification of BMP and Activin Membrane-Bound Inhibitor (BAMBI) as a Potent Negative Regulator of Adipogenesis and Modulator of Autocrine/Paracrine Adipogenic Factors.</title>
            <link>http://www.medworm.com/index.php?rid=5538088&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22187378%26dopt%3DAbstract</link>
            <description>Authors: Luo X, Hutley LJ, Webster JA, Kim YH, Liu DF, Newell FS, Widberg CH, Bachmann A, Turner N, Schmitz-Peiffer C, Prins JB, Yang GS, Whitehead JP
    Abstract
    Adipose tissue dysfunction underpins the association of obesity with type 2 diabetes. Adipogenesis is required for the maintenance of adipose tissue function. It involves the commitment and subsequent differentiation of preadipocytes and is coordinated by autocrine, paracrine, and endocrine factors. We previously reported that fibroblast growth factor-1 (FGF-1) primes primary human preadipocytes and Simpson Golabi Behmel syndrome (SGBS) preadipocytes and increases adipogenesis through a cascade involving extracellular signal-related kinase 1/2 (ERK1/2). Here, we aimed to use the FGF-1 system to identify novel adipogenic regu...</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538088</comments>
            <pubDate>Sun, 25 Dec 2011 06:07:46 +0100</pubDate>
            <guid isPermaLink="false">5538088</guid>        </item>
        <item>
            <title>Nerve growth factor gene therapy using adeno-associated viral vectors prevents cardiomyopathy in type 1 diabetic mice.</title>
            <link>http://www.medworm.com/index.php?rid=5538087&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22187379%26dopt%3DAbstract</link>
            <description>This study investigated whether NGF gene transfer can prevent diabetic cardiomyopathy in mice. We worked with mice with streptozotocin-induced type 1 diabetes and with nondiabetic control mice. After having established that diabetes reduces cardiac NGF mRNA expression, we tested NGF gene therapies with adeno-associated viral vectors (AAVs) for the capacity to protect the diabetic mouse heart. To this aim, after 2 weeks of diabetes, cardiac expression of human NGF or β-Gal (control) genes was induced by either intramyocardial injection of AAV serotype 2 (AAV2) or systemic delivery of AAV serotype 9 (AAV9). Nondiabetic mice were given AAV2-β-Gal or AAV9-β-Gal. We found that the diabetic mice receiving NGF gene transfer via either AAV2 or AAV9 were spared the progressive deterioration of c...</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538087</comments>
            <pubDate>Sun, 25 Dec 2011 06:07:36 +0100</pubDate>
            <guid isPermaLink="false">5538087</guid>        </item>
        <item>
            <title>The ATP-Sensitive K+ Channel ABCC8 S1369A Type 2 Diabetes Risk Variant Increases MgATPase Activity.</title>
            <link>http://www.medworm.com/index.php?rid=5538086&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22187380%26dopt%3DAbstract</link>
            <description>Authors: Fatehi M, Raja M, Carter C, Soliman D, Holt A, Light PE
    Abstract
    Pancreatic β-cell ATP-sensitive K(+) (K(ATP)) channels are composed of Kir6.2 and SUR1 subunits encoded by the KCNJ11 and ABCC8 genes, respectively. Although rare monogenic activating mutations in these genes cause overt neonatal diabetes, the common variants E23K (KCNJ11) and S1369A (ABCC8) form a tightly heritable haplotype that is associated with an increased susceptibility to type 2 diabetes (T2D) risk. However, the molecular mechanism(s) underlying this risk remain to be elucidated. A homology model of the SUR1 nucleotide-binding domains (NBDs) indicates that residue 1369 is in close proximity to the major MgATPase site. Therefore, we investigated the intrinsic MgATPase activity of K(ATP) channels conta...</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538086</comments>
            <pubDate>Sun, 25 Dec 2011 06:07:26 +0100</pubDate>
            <guid isPermaLink="false">5538086</guid>        </item>
        <item>
            <title>Issues and events.</title>
            <link>http://www.medworm.com/index.php?rid=5538085&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22187381%26dopt%3DAbstract</link>
            <description>Authors: 
    PMID: 22187381 [PubMed - in process] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538085</comments>
            <pubDate>Sun, 25 Dec 2011 06:07:15 +0100</pubDate>
            <guid isPermaLink="false">5538085</guid>        </item>
        <item>
            <title>Comment on: Maruthur et al. Does Genetic Ancestry Explain Higher Values of Glycated Hemoglobin in African Americans? Diabetes 2011;60:2434-2438.</title>
            <link>http://www.medworm.com/index.php?rid=5538084&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22187382%26dopt%3DAbstract</link>
            <description>Authors: Dagogo-Jack S
    PMID: 22187382 [PubMed - in process] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538084</comments>
            <pubDate>Sun, 25 Dec 2011 06:07:05 +0100</pubDate>
            <guid isPermaLink="false">5538084</guid>        </item>
        <item>
            <title>Response to Comment on: Maruthur et al. Does Genetic Ancestry Explain Higher Values of Glycated Hemoglobin in African Americans? Diabetes 2011;60:2434-2438.</title>
            <link>http://www.medworm.com/index.php?rid=5538083&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22187383%26dopt%3DAbstract</link>
            <description>Authors: Maruthur NM, Kao WH, Selvin E
    PMID: 22187383 [PubMed - in process] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538083</comments>
            <pubDate>Sun, 25 Dec 2011 06:06:55 +0100</pubDate>
            <guid isPermaLink="false">5538083</guid>        </item>
        <item>
            <title>Increased Macrophage Migration Into Adipose Tissue in Obese Mice.</title>
            <link>http://www.medworm.com/index.php?rid=5538082&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22190646%26dopt%3DAbstract</link>
            <description>We report a new method to quantitate in vivo macrophage tracking (i.e., blood monocytes from donor mice) labeled ex vivo with fluorescent PKH26 dye and injected into recipient mice. Labeled monocytes appear as adipose, liver, and splenic macrophages, peaking in 1-2 days. When CCR2 KO monocytes are injected into wild-type (WT) recipients, or WT monocytes given to MCP-1 KO recipients, adipose tissue macrophage (ATM) accumulation is reduced by ~40%, whereas hepatic macrophage content is decreased by ~80%. Using WT donor cells, ATM accumulation is several-fold greater in obese recipient mice compared with lean mice, regardless of the source of donor monocytes. After their appearance in adipose tissue, ATMs progressively polarize from the M2- to the M1-like state in obesity. In summary, the CCR...</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538082</comments>
            <pubDate>Wed, 21 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538082</guid>        </item>
        <item>
            <title>Complete Diabetes Protection Despite Delayed Thymic Tolerance in NOD8.3 TCR Transgenic Mice Due to Antigen-Induced Extrathymic Deletion of T Cells.</title>
            <link>http://www.medworm.com/index.php?rid=5538081&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22190647%26dopt%3DAbstract</link>
            <description>Authors: Krishnamurthy B, Chee J, Jhala G, Fynch S, Graham KL, Santamaria P, Morahan G, Allison J, Izon D, Thomas HE, Kay TW
    Abstract
    Prevention of autoimmunity requires the elimination of self-reactive T cells during their development in the thymus and maturation in the periphery. Transgenic NOD mice that overexpress islet-specific glucose 6 phosphatase catalytic subunit related protein (IGRP) in antigen-presenting cells (NOD-IGRP mice) have no IGRP-specific T cells. To study the relative contribution of central and peripheral tolerance mechanisms to deletion of antigen-specific T cells, we crossed NOD-IGRP mice to highly diabetogenic IGRP(206-214) T-cell receptor transgenic mice (NOD8.3 mice) and studied the frequency and function of IGRP-specific T cells in the thymus and periph...</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538081</comments>
            <pubDate>Wed, 21 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538081</guid>        </item>
        <item>
            <title>Short-Chain Fatty Acids Stimulate Glucagon-Like Peptide-1 Secretion via the G-Protein-Coupled Receptor FFAR2.</title>
            <link>http://www.medworm.com/index.php?rid=5538080&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22190648%26dopt%3DAbstract</link>
            <description>Authors: Tolhurst G, Heffron H, Lam YS, Parker HE, Habib AM, Diakogiannaki E, Cameron J, Grosse J, Reimann F, Gribble FM
    Abstract
    Interest in how the gut microbiome can influence the metabolic state of the host has recently heightened. One postulated link is bacterial fermentation of &quot;indigestible&quot; prebiotics to short-chain fatty acids (SCFAs), which in turn modulate the release of gut hormones controlling insulin release and appetite. We show here that SCFAs trigger secretion of the incretin hormone glucagon-like peptide (GLP)-1 from mixed colonic cultures in vitro. Quantitative PCR revealed enriched expression of the SCFA receptors ffar2 (grp43) and ffar3 (gpr41) in GLP-1-secreting L cells, and consistent with the reported coupling of GPR43 to Gq signaling pathways, SCFAs raised ...</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538080</comments>
            <pubDate>Wed, 21 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538080</guid>        </item>
        <item>
            <title>Postnatal Growth and DNA Methylation Are Associated With Differential Gene Expression of the TACSTD2 Gene and Childhood Fat Mass.</title>
            <link>http://www.medworm.com/index.php?rid=5538079&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22190649%26dopt%3DAbstract</link>
            <description>Authors: Groom A, Potter C, Swan DC, Fatemifar G, Evans DM, Ring SM, Turcot V, Pearce MS, Embleton ND, Davey G, Smith , Mathers JC, Relton CL
    Abstract
    Rapid postnatal growth is associated with increased risk of childhood adiposity. The aim of this study was to establish whether this pathway is mediated by altered DNA methylation and gene expression. Two distinct cohorts, one preterm (n = 121) and one term born (n = 6,990), were studied. Exploratory analyses were performed using microarrays to identify differentially expressed genes in whole blood from children defined as &quot;slow&quot; (n = 10) compared with &quot;rapid&quot; (n = 10) postnatal (term to 12 weeks corrected age) growers. Methylation within the identified TACSTD2 gene was measured in both cohorts, and rs61779296 genotype was determined...</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538079</comments>
            <pubDate>Wed, 21 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538079</guid>        </item>
        <item>
            <title>The L-α-Lysophosphatidylinositol/GPR55 System and Its Potential Role in Human Obesity.</title>
            <link>http://www.medworm.com/index.php?rid=5538100&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22179809%26dopt%3DAbstract</link>
            <description>Authors: Moreno-Navarrete JM, Catalán V, Whyte L, Díaz-Arteaga A, Vázquez-Martínez R, Rotellar F, Guzmán R, Gómez-Ambrosi J, Pulido MR, Russell WR, Imbernón M, Ross RA, Malagón MM, Dieguez C, Fernández-Real JM, Frühbeck G, Nogueiras R
    Abstract
    GPR55 is a putative cannabinoid receptor, and L-α-lysophosphatidylinositol (LPI) is its only known endogenous ligand. We investigated 1) whether GPR55 is expressed in fat and liver; 2) the correlation of both GPR55 and LPI with several metabolic parameters; and 3) the actions of LPI on human adipocytes. We analyzed CB1, CB2, and GPR55 gene expression and circulating LPI levels in two independent cohorts of obese and lean subjects, with both normal or impaired glucose tolerance and type 2 diabetes. Ex vivo experiments were used to m...</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538100</comments>
            <pubDate>Fri, 16 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538100</guid>        </item>
        <item>
            <title>Glucose-Dependent Insulinotropic Polypeptide Reduces Fat-Specific Expression and Activity of 11β-Hydroxysteroid Dehydrogenase Type 1 and Inhibits Release of Free Fatty Acids.</title>
            <link>http://www.medworm.com/index.php?rid=5538099&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22179810%26dopt%3DAbstract</link>
            <description>Authors: Gögebakan O, Andres J, Biedasek K, Mai K, Kühnen P, Krude H, Isken F, Rudovich N, Osterhoff MA, Kintscher U, Nauck M, Pfeiffer AF, Spranger J
    Abstract
    Glucose-dependent insulinotropic polypeptide (GIP) has been suggested to have direct effects on nonislet tissues. GIP also reportedly increased glucose uptake and inhibition of lipolysis in adipocytes after inhibition of the intracellular cortisone-cortisol shuttle 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1). We here analyzed whether GIP modifies lipid metabolism and further elucidated the relation between GIP, 11β-HSD1, and fatty acid metabolism. GIP reduced activity of 11β-HSD1 promoter constructs and the expression and activity of 11β-HSD1 in differentiated 3T3-L1 adipocytes in a time- and dose-dependent fas...</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538099</comments>
            <pubDate>Fri, 16 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538099</guid>        </item>
        <item>
            <title>Farewell statement from dr. Peter butler as outgoing editor in chief of diabetes.</title>
            <link>http://www.medworm.com/index.php?rid=5478556&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22110090%26dopt%3DAbstract</link>
            <description>Authors: Butler PC
    PMID: 22110090 [PubMed - in process] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5478556</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5478556</guid>        </item>
        <item>
            <title>SirT1: A Guardian at the Gates of Adipose Tissue Inflammation.</title>
            <link>http://www.medworm.com/index.php?rid=5478555&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22110091%26dopt%3DAbstract</link>
            <description>Authors: Cho KW, Lumeng CN
    PMID: 22110091 [PubMed - in process] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5478555</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5478555</guid>        </item>
        <item>
            <title>SirT1 Regulates Adipose Tissue Inflammation.</title>
            <link>http://www.medworm.com/index.php?rid=5478554&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22110092%26dopt%3DAbstract</link>
            <description>CONCLUSIONS Reduction of adipose tissue SirT1 expression, which leads to histone hyperacetylation and ectopic inflammatory gene expression, is identified as a key regulatory component of macrophage influx into adipose tissue during overnutrition in rodents and humans. Our results suggest that SirT1 regulates adipose tissue inflammation by controlling the gain of proinflammatory transcription in response to inducers such as fatty acids, hypoxia, and endoplasmic reticulum stress.
    PMID: 22110092 [PubMed - in process] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5478554</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5478554</guid>        </item>
        <item>
            <title>Cesarean section and interferon-induced helicase gene polymorphisms combine to increase childhood type 1 diabetes risk.</title>
            <link>http://www.medworm.com/index.php?rid=5478553&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22110093%26dopt%3DAbstract</link>
            <description>CONCLUSIONS These findings suggest that type 1 diabetes risk modification by cesarean section may be linked to viral responses in the preclinical autoantibody-positive disease phase.
    PMID: 22110093 [PubMed - in process] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5478553</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5478553</guid>        </item>
        <item>
            <title>Issues and events.</title>
            <link>http://www.medworm.com/index.php?rid=5478552&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22110094%26dopt%3DAbstract</link>
            <description>Authors: 
    PMID: 22110094 [PubMed - in process] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5478552</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5478552</guid>        </item>
        <item>
            <title>Maternal Serum Levels of 25-Hydroxy-Vitamin D During Pregnancy and Risk of Type 1 Diabetes in the Offspring.</title>
            <link>http://www.medworm.com/index.php?rid=5478551&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22124461%26dopt%3DAbstract</link>
            <description>Authors: Sørensen IM, Joner G, Jenum PA, Eskild A, Torjesen PA, Stene LC
    Abstract
    Previous studies indicate reduced risk of type 1 diabetes after intake of vitamin D supplements during pregnancy or early childhood. We aimed to test whether lower maternal serum concentrations of 25-hydroxy-vitamin D (25-OH D) during pregnancy were associated with an increased risk of childhood-onset type 1 diabetes. In this case-control study nested within a cohort of 29,072 women in Norway, 25-OH D levels were measured using a radioimmunoassay on samples from late pregnancy in 109 women delivering a child who developed type 1 diabetes before 15 years of age (case subjects) and from 219 control women. Dividing the levels of maternal 25-OH D into quartiles, there was a trend toward a higher risk of ...</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5478551</comments>
            <pubDate>Mon, 28 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5478551</guid>        </item>
        <item>
            <title>Distinguishing Persistent Insulin Autoantibodies With Differential Risk: Nonradioactive Bivalent Proinsulin/Insulin Autoantibody Assay.</title>
            <link>http://www.medworm.com/index.php?rid=5478550&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22124462%26dopt%3DAbstract</link>
            <description>Authors: Yu L, Miao D, Scrimgeour L, Johnson K, Rewers M, Eisenbarth GS
    Abstract
    A subset of children develops persistent insulin autoantibodies (IAA; almost always as the only islet autoantibody) without evidence of progression to diabetes. The aim of the current study was the development and characterization of the performance of a nonradioactive fluid phase insulin autoantibody assay in relation to standard IAA radioassay. We developed a nonradioactive IAA assay where bivalent IAA cross-link two insulin moieties in a fluid phase. The serum samples positive for anti-islet autoantibodies from 150 newly diagnosed patients with diabetes (Barbara Davis Center plus Diabetes Autoantibody Standardization Program [DASP] Workshop) and 70 prediabetic subjects who were followed to diabetes ...</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5478550</comments>
            <pubDate>Mon, 28 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5478550</guid>        </item>
        <item>
            <title>Sirtuin 1-Mediated Cellular Metabolic Memory of High Glucose Via the LKB1/AMPK/ROS Pathway and Therapeutic Effects of Metformin.</title>
            <link>http://www.medworm.com/index.php?rid=5478549&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22124463%26dopt%3DAbstract</link>
            <description>Authors: Zheng Z, Chen H, Li J, Li T, Zheng B, Zheng Y, Jin H, He Y, Gu Q, Xu X
    Abstract
    Cellular metabolic memory occurs in diabetic microvascular and macrovascular complications, but the underlying mechanisms remain unclear. Here, we investigate the role of sirtuin 1 (SIRT1) and metformin in this phenomenon. In bovine retinal capillary endothelial cells (BRECs) and retinas of diabetic rats, the inflammatory gene, nuclear factor-κB (NF-kB), and the proapoptotic gene, Bax, induced by hyperglycemia, remained elevated after returning to normoglycemia. BRECs with small interfering RNA-mediated SIRT1 knockdown had increased sensitivity to hyperglycemia stress, whereas SIRT1 overexpression or activation by metformin inhibited the increase of mitochondrial reactive oxygen species-mediat...</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5478549</comments>
            <pubDate>Mon, 28 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5478549</guid>        </item>
        <item>
            <title>Endoplasmic Reticulum Stress Inhibits STAT3-Dependent Suppression of Hepatic Gluconeogenesis via Dephosphorylation and Deacetylation.</title>
            <link>http://www.medworm.com/index.php?rid=5478548&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22124464%26dopt%3DAbstract</link>
            <description>Authors: Kimura K, Yamada T, Kaneko S, Matsumoto M, Kido Y, Hosooka T, Asahara SI, Matsuda T, Ota T, Watanabe H, Sai Y, Miyamoto K, Kasuga M, Inoue H
    Abstract
    In the liver, signal transducer and activator of transcription 3 (STAT3) plays an important role in the suppression of gluconeogenic enzyme expression. While obesity-associated endoplasmic reticulum (ER) stress has been shown to increase hepatic gluconeogenic enzyme expression, the role of ER stress in STAT3-dependent regulation of such expression is unclear. The current study aimed to elucidate the effect of ER stress on the STAT3-dependent regulation of hepatic gluconeogenic enzyme expression. Genetically obese/diabetic db/db mice and db/db mouse-derived isolated hepatocytes were used as ER stress models. A tyrosine phospha...</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5478548</comments>
            <pubDate>Mon, 28 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5478548</guid>        </item>
        <item>
            <title>Na+-d-glucose Cotransporter SGLT1 is Pivotal for Intestinal Glucose Absorption and Glucose-Dependent Incretin Secretion.</title>
            <link>http://www.medworm.com/index.php?rid=5478547&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22124465%26dopt%3DAbstract</link>
            <description>Authors: Gorboulev V, Schürmann A, Vallon V, Kipp H, Jaschke A, Klessen D, Friedrich A, Scherneck S, Rieg T, Cunard R, Veyhl-Wichmann M, Srinivasan A, Balen D, Breljak D, Rexhepaj R, Parker HE, Gribble FM, Reimann F, Lang F, Wiese S, Sabolic I, Sendtner M, Koepsell H
    Abstract
    To clarify the physiological role of Na(+)-d-glucose cotransporter SGLT1 in small intestine and kidney, Sglt1(-/-) mice were generated and characterized phenotypically. After gavage of d-glucose, small intestinal glucose absorption across the brush-border membrane (BBM) via SGLT1 and GLUT2 were analyzed. Glucose-induced secretion of insulinotropic hormone (GIP) and glucagon-like peptide 1 (GLP-1) in wild-type and Sglt1(-/-) mice were compared. The impact of SGLT1 on renal glucose handling was investigated by ...</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5478547</comments>
            <pubDate>Mon, 28 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5478547</guid>        </item>
        <item>
            <title>In Vivo Adipogenesis in Rats Measured by Cell Kinetics in Adipocytes and Plastic-Adherent Stroma-Vascular Cells in Response to High-Fat Diet and Thiazolidinedione.</title>
            <link>http://www.medworm.com/index.php?rid=5478546&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22124466%26dopt%3DAbstract</link>
            <description>Authors: Tchoukalova YD, Fitch M, Rogers PM, Covington JD, Henagan TM, Ye J, Hellerstein MK, Ravussin E
    Abstract
    Impairment of adipogenesis contributes to the development of obesity-related insulin resistance. The current in vitro approaches for its assessment represent crude estimates of the adipogenic potential because of the disruption of the in vivo microenvironment. A novel assessment of in vivo adipogenesis using the incorporation of the stable isotope deuterium ((2)H) into the DNA of isolated adipocytes and stroma-vascular fraction from adipose tissue has been developed. In the current study, we have refined this technique by purifying the adipocytes via a negative immune selection and sorting the plastic adherent stroma-vascular (aSV) subfraction (using 3 h culture) that co...</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5478546</comments>
            <pubDate>Mon, 28 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5478546</guid>        </item>
        <item>
            <title>Cellular Mechanisms of Restored β-Cell Tolerance Mediated by Protective Alleles of Idd3 and Idd5.</title>
            <link>http://www.medworm.com/index.php?rid=5478564&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22106155%26dopt%3DAbstract</link>
            <description>Authors: Hamilton-Williams EE, Cheung J, Rainbow DB, Hunter KM, Wicker LS, Sherman LA
    Abstract
    Type 1 diabetes genes within the IL-2, CTLA-4, and NRAMP1 pathways influence development of autoimmune diabetes in humans and NOD mice. In NOD mice, when present together, protective alleles encoding interleukin-2 (IL-2), Idd3 candidate gene, CTLA-4, NRAMP1, and ACADL (candidate genes for the Idd5.1, Idd5.2, and Idd5.3 subregions) provide nearly complete diabetes protection. To define where the protective alleles of Idd3 and the Idd5 subregions must be present to protect from diabetes and tolerize islet-specific CD8(+) T cells, SCID mice were reconstituted so that the host and lymphocytes expressed various combinations of protective and susceptibility alleles at Idd3 and Idd5. Although pr...</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5478564</comments>
            <pubDate>Mon, 21 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5478564</guid>        </item>
        <item>
            <title>A Novel Mechanism for Regulating Hepatic Glycogen Synthesis Involving Serotonin and Cyclin-Dependent Kinase-5.</title>
            <link>http://www.medworm.com/index.php?rid=5478563&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22106156%26dopt%3DAbstract</link>
            <description>Authors: Tudhope SJ, Wang CC, Petrie JL, Potts L, Malcomson F, Kieswich J, Yaqoob MM, Arden C, Hampson LJ, Agius L
    Abstract
    Hepatic autonomic nerves regulate postprandial hepatic glucose uptake but the signaling pathways remain unknown. We tested the hypothesis that serotonin (5-hydroxytryptamine [5-HT]) exerts stimulatory and inhibitory effects on hepatic glucose disposal. Ligands of diverse 5-HT receptors were used to identify signaling pathway(s) regulating glucose metabolism in hepatocytes. 5-HT had stimulatory and inhibitory effects on glycogen synthesis in hepatocytes mediated by 5-HT1/2A and 5-HT2B receptors, respectively. Agonists of 5-HT1/2A receptors lowered blood glucose and increased hepatic glycogen after oral glucose loading, and stimulated glycogen synthesis in fresh...</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5478563</comments>
            <pubDate>Mon, 21 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5478563</guid>        </item>
        <item>
            <title>Greater Impact of Melanocortin-4 Receptor Deficiency on Rates of Growth and Risk of Type 2 Diabetes Mellitus During Childhood Compared With Adulthood in Pima Indians.</title>
            <link>http://www.medworm.com/index.php?rid=5478560&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22106157%26dopt%3DAbstract</link>
            <description>Authors: Thearle MS, Muller YL, Hanson RL, Mullins M, Abdussamad M, Tran J, Knowler WC, Bogardus C, Krakoff J, Baier LJ
    Abstract
    Features of melanocortin-4 receptor (MC4R) deficiency have been observed to be more pronounced in childhood. Longitudinal data from a population-based study were used to separate the phenotypic effects of MC4R deficiency during childhood and adulthood. The MC4R exon was sequenced in 6,760 individuals of predominantly Pima Indian heritage, and discovered mutations were functionally assessed in vitro. Effects on BMI, height, and slope of BMI change were assessed during childhood (ages 5-20 years) and adulthood (ages 20-45 years). Six mutations affecting MC4R function, including three that may be private to Pima Indians, were found in 159 individuals (2.4%)....</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5478560</comments>
            <pubDate>Mon, 21 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5478560</guid>        </item>
        <item>
            <title>Relative Expression of a Dominant Mutated ABCC8 Allele Determines the Clinical Manifestation of Congenital Hyperinsulinism.</title>
            <link>http://www.medworm.com/index.php?rid=5478559&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22106158%26dopt%3DAbstract</link>
            <description>In conclusion, differences in transcript expression may determine the clinical phenotype of CHI in this maternally inherited dominant mutation. The use of peripheral lymphocytes as a peripheral window to the β-cell transcription profile can serve in resolving β-cell phenotypes. The severe, dominant-negative nature of the 1508insAS mutation suggests that it affects the functional stoichiometry of SUR1-regulated gating of K(ATP) channels.
    PMID: 22106158 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5478559</comments>
            <pubDate>Mon, 21 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5478559</guid>        </item>
        <item>
            <title>Somatostatin Receptor Type 2 Antagonism Improves Glucagon and Corticosterone Counterregulatory Responses to Hypoglycemia in Streptozotocin-Induced Diabetic Rats.</title>
            <link>http://www.medworm.com/index.php?rid=5478558&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22106159%26dopt%3DAbstract</link>
            <description>Authors: Yue JT, Burdett E, Coy DH, Giacca A, Efendic S, Vranic M
    Abstract
    Diminished responsiveness to hypoglycemia contributes to defective counterregulation in diabetes. Pancreatic and/or circulating somatostatin are elevated in diabetes, which may inhibit counterregulatory hormone release during hypoglycemia. Thus, a selective somatostatin receptor type 2 antagonist (SSTR2a) should improve hormone counterregulation to hypoglycemia. Nondiabetic (N) and streptozotocin-induced diabetic (D) rats underwent 4-h infusion of saline or SSTR2a with insulin-induced hypoglycemia clamped at 2.5 ± 0.5 mmol/L. To evaluate the effect of the SSTR2a in the absence of hypoglycemia, rats underwent a 4-h infusion of saline (Ctrl:N, Ctrl:D) or SSTR2a (Ctrl:D+SSTR2a) only. The attenuated glucagon re...</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5478558</comments>
            <pubDate>Mon, 21 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5478558</guid>        </item>
        <item>
            <title>Heparanase Is Essential for the Development of Diabetic Nephropathy in Mice.</title>
            <link>http://www.medworm.com/index.php?rid=5478557&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22106160%26dopt%3DAbstract</link>
            <description>We report for the first time the essential involvement of heparanase in DN. With the use of Hpse-KO mice, we found that deletion of the heparanase gene protects diabetic mice from DN. Furthermore, by investigating the molecular mechanism underlying induction of the enzyme in DN, we found that transcription factor early growth response 1 is responsible for activation of heparanase promoter under diabetic conditions. The specific heparanase inhibitor SST0001 markedly decreased the extent of albuminuria and renal damage in mouse models of DN. Our results collectively underscore the crucial role of heparanase in the pathogenesis of DN and its potential as a highly relevant target for therapeutic interventions in patients with DN.
    PMID: 22106160 [PubMed - as supplied by publisher] (Source: ...</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5478557</comments>
            <pubDate>Mon, 21 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5478557</guid>        </item>
        <item>
            <title>Reproductive Tissues Maintain Insulin Sensitivity in Diet-Induced Obesity.</title>
            <link>http://www.medworm.com/index.php?rid=5427195&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22076926%26dopt%3DAbstract</link>
            <description>Authors: Wu S, Divall S, Wondisford F, Wolfe A
    Abstract
    Reproductive dysfunction is associated with obesity. We previously showed that female mice with diet-induced obesity (DIO) exhibit infertility and thus serve as a model of human polycystic ovary syndrome (PCOS). We postulated that differential insulin signaling of tissues leads to reproductive dysfunction; therefore, a comparison of insulin signaling in reproductive tissues and energy storage tissues was performed. Pituitary-specific insulin receptor knockout mice were used as controls. High-fat diet-induced stress, which leads to insulin resistance, was also investigated by assaying macrophage infiltration and phosphorylated Jun NH(2)-terminal kinase (pJNK) signaling. In lean mice, reproductive tissues exhibited reduced sensi...</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5427195</comments>
            <pubDate>Thu, 10 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5427195</guid>        </item>
        <item>
            <title>Inotuzumab Ozogamicin Murine Analog-Mediated B-Cell Depletion Reduces Anti-Islet Allo- and Autoimmune Responses.</title>
            <link>http://www.medworm.com/index.php?rid=5427194&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22076927%26dopt%3DAbstract</link>
            <description>Authors: Carvello M, Petrelli A, Vergani A, Lee KM, Tezza S, Chin M, Orsenigo E, Staudacher C, Secchi A, Dunussi-Joannopoulos K, Sayegh MH, Markmann JF, Fiorina P
    Abstract
    B cells participate in the priming of the allo- and autoimmune responses, and their depletion can thus be advantageous for islet transplantation. Herein, we provide an extensive study of the effect of B-cell depletion in murine models of islet transplantation. Islet transplantation was performed in hyperglycemic B-cell-deficient (μMT) mice, in a purely alloimmune setting (BALB/c into hyperglycemic C57BL/6), in a purely autoimmune setting (NOD.SCID into hyperglycemic NOD), and in a mixed allo-/autoimmune setting (BALB/c into hyperglycemic NOD). Inotuzumab ozogamicin murine analog (anti-CD22 monoclonal antibody co...</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5427194</comments>
            <pubDate>Thu, 10 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5427194</guid>        </item>
        <item>
            <title>Poverty and obesity in the u.s.</title>
            <link>http://www.medworm.com/index.php?rid=5383175&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22025771%26dopt%3DAbstract</link>
            <description>Authors: Levine JA
    PMID: 22025771 [PubMed - in process] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5383175</comments>
            <pubDate>Tue, 01 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5383175</guid>        </item>
        <item>
            <title>It's Time to Mow the GRAS in Type 1 Diabetes.</title>
            <link>http://www.medworm.com/index.php?rid=5383174&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22025772%26dopt%3DAbstract</link>
            <description>Authors: Schatz DA, Levine SR, Atkinson MA
    PMID: 22025772 [PubMed - in process] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5383174</comments>
            <pubDate>Tue, 01 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5383174</guid>        </item>
        <item>
            <title>Artificial pancreas: past, present, future.</title>
            <link>http://www.medworm.com/index.php?rid=5383173&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22025773%26dopt%3DAbstract</link>
            <description>Authors: Cobelli C, Renard E, Kovatchev B
    PMID: 22025773 [PubMed - in process] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5383173</comments>
            <pubDate>Tue, 01 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5383173</guid>        </item>
        <item>
            <title>Nrf2 activators as attractive therapeutics for diabetic nephropathy.</title>
            <link>http://www.medworm.com/index.php?rid=5383172&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22025774%26dopt%3DAbstract</link>
            <description>Authors: de Haan JB
    PMID: 22025774 [PubMed - in process] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5383172</comments>
            <pubDate>Tue, 01 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5383172</guid>        </item>
        <item>
            <title>FUT2 Nonfunctional Variant: A &quot;Missing Link&quot; Between Genes and Environment in Type 1 Diabetes?</title>
            <link>http://www.medworm.com/index.php?rid=5383171&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22025775%26dopt%3DAbstract</link>
            <description>FUT2 Nonfunctional Variant: A &quot;Missing Link&quot; Between Genes and Environment in Type 1 Diabetes?
    Diabetes. 2011 Nov;60(11):2685-7
    Authors: Yang P, Li HL, Wang CY
    PMID: 22025775 [PubMed - in process] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5383171</comments>
            <pubDate>Tue, 01 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5383171</guid>        </item>
        <item>
            <title>Metabolomics makes a mark: early changes associated with autoimmune diabetes.</title>
            <link>http://www.medworm.com/index.php?rid=5383170&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22025776%26dopt%3DAbstract</link>
            <description>Authors: Leslie RD, Beyan H
    PMID: 22025776 [PubMed - in process] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5383170</comments>
            <pubDate>Tue, 01 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5383170</guid>        </item>
        <item>
            <title>Age- and islet autoimmunity-associated differences in amino Acid and lipid metabolites in children at risk for type 1 diabetes.</title>
            <link>http://www.medworm.com/index.php?rid=5383169&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22025777%26dopt%3DAbstract</link>
            <description>CONCLUSIONS Distinct metabolic profiles are associated with age and islet autoimmunity. Pathways that use methionine are potentially relevant for developing islet autoantibodies in early infancy.
    PMID: 22025777 [PubMed - in process] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5383169</comments>
            <pubDate>Tue, 01 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5383169</guid>        </item>
        <item>
            <title>Subcutaneous Adipose Tissue Macrophage Infiltration Is Associated With Hepatic and Visceral Fat Deposition, Hyperinsulinemia, and Stimulation of NF-{kappa}B Stress Pathway.</title>
            <link>http://www.medworm.com/index.php?rid=5383168&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22025778%26dopt%3DAbstract</link>
            <description>CONCLUSIONS Adipose tissue inflammation was equally distributed between sexes and ethnicities. It was associated with partitioning of fat toward VAT and the liver and altered β-cell function, independent of total adiposity. Several genes belonging to the NF-κB stress pathway were upregulated, suggesting stimulation of proinflammatory mediators.
    PMID: 22025778 [PubMed - in process] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5383168</comments>
            <pubDate>Tue, 01 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5383168</guid>        </item>
        <item>
            <title>Therapeutic potential of nrf2 activators in streptozotocin-induced diabetic nephropathy.</title>
            <link>http://www.medworm.com/index.php?rid=5383167&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22025779%26dopt%3DAbstract</link>
            <description>CONCLUSIONS We provide experimental evidence indicating that dietary compounds targeting Nrf2 activation can be used therapeutically to improve metabolic disorder and relieve renal damage induced by diabetes.
    PMID: 22025779 [PubMed - in process] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5383167</comments>
            <pubDate>Tue, 01 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5383167</guid>        </item>
        <item>
            <title>FUT2 Nonsecretor Status Links Type 1 Diabetes Susceptibility and Resistance to Infection.</title>
            <link>http://www.medworm.com/index.php?rid=5383166&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22025780%26dopt%3DAbstract</link>
            <description>CONCLUSIONS Our findings linking FUT2 and type 1 diabetes highlight the intriguing relationship between host resistance to infections and susceptibility to autoimmune disease.
    PMID: 22025780 [PubMed - in process] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5383166</comments>
            <pubDate>Tue, 01 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5383166</guid>        </item>
        <item>
            <title>Issues and events.</title>
            <link>http://www.medworm.com/index.php?rid=5383165&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22025781%26dopt%3DAbstract</link>
            <description>Authors: 
    PMID: 22025781 [PubMed - in process] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5383165</comments>
            <pubDate>Tue, 01 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5383165</guid>        </item>
        <item>
            <title>Synergistic Reversal of Type 1 Diabetes in NOD Mice With Anti-CD3 and Interleukin-1 Blockade: Evidence of Improved Immune Regulation.</title>
            <link>http://www.medworm.com/index.php?rid=5383161&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22043003%26dopt%3DAbstract</link>
            <description>Authors: Ablamunits V, Henegariu O, Hansen JB, Opare-Addo L, Preston-Hurlburt P, Santamaria P, Mandrup-Poulsen T, Herold KC
    Abstract
    Inflammatory cytokines are involved in autoimmune diabetes: among the most prominent is interleukin (IL)-1β. We postulated that blockade of IL-1β would modulate the effects of anti-CD3 monoclonal antibody (mAb) in treating diabetes in NOD mice. To test this, we treated hyperglycemic NOD mice with F(ab')(2) fragments of anti-CD3 mAb with or without IL-1 receptor antagonist (IL-1RA), or anti-IL-1β mAb. We studied the reversal of diabetes and effects of treatment on the immune system. Mice that received a combination of anti-CD3 mAb with IL-1RA showed a more rapid rate of remission of diabetes than mice treated with anti-CD3 mAb or IL-1RA alone. Combi...</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5383161</comments>
            <pubDate>Mon, 31 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5383161</guid>        </item>
        <item>
            <title>Gipr Is Essential for Adrenocortical Steroidogenesis; However, Corticosterone Deficiency Does Not Mediate the Favorable Metabolic Phenotype of Gipr-/- Mice.</title>
            <link>http://www.medworm.com/index.php?rid=5383160&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22043004%26dopt%3DAbstract</link>
            <description>Authors: Bates HE, Campbell JE, Usher JR, Baggio LL, Maida A, Seino Y, Drucker DJ
    Abstract
    Glucose-dependent insulinotropic polypeptide (GIP) promotes glucose-dependent insulin secretion. However, GIP also enhances glucocorticoid secretion and promotes adiposity. Because obesity and diabetes are glucocorticoid dependent, we examined whether the effects of GIP on energy balance and glycemia are regulated by glucocorticoids using pharmacological activation of GIP receptor (GIPR) signaling with [D-Ala(2)]GIP in mice and in Y1 adrenocortical cells. Genetic elimination of GIPR activity was also studied in normal- and high fat (HF)-fed Gipr deficient (Gipr(-/-)) mice. [D-Ala(2)]GIP increased murine corticosterone levels in a GIPR-dependent manner. Conversely, basal corticosterone levels ...</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5383160</comments>
            <pubDate>Mon, 31 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5383160</guid>        </item>
        <item>
            <title>Glucagon-Like Peptide 1 Inhibits the Sirtuin Deacetylase SirT1 to Stimulate Pancreatic β-Cell Mass Expansion.</title>
            <link>http://www.medworm.com/index.php?rid=5383179&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22013015%26dopt%3DAbstract</link>
            <description>CONCLUSIONOur study shows for the first time that the glucoincretin hormone GLP-1 modulates SirT1 activity and FoxO1 acetylation in β-cells. We also identify SirT1 as a negative regulator of β-cell proliferation.
    PMID: 22013015 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5383179</comments>
            <pubDate>Tue, 25 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5383179</guid>        </item>
        <item>
            <title>Influence of Hyperinsulinemia and Insulin Resistance on In Vivo β-Cell Function: Their Role in Human β-Cell Dysfunction.</title>
            <link>http://www.medworm.com/index.php?rid=5383164&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22028180%26dopt%3DAbstract</link>
            <description>CONCLUSIONSPre-exposure to physiological hyperinsulinemia stimulates insulin secretion to a degree that depends on insulin sensitivity. However, this phenomenon has limited impact on β-cell dysfunction and dysglycemia.
    PMID: 22028180 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5383164</comments>
            <pubDate>Tue, 25 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5383164</guid>        </item>
        <item>
            <title>Susceptibility of Glucokinase-MODY Mutants to Inactivation by Oxidative Stress in Pancreatic β-Cells.</title>
            <link>http://www.medworm.com/index.php?rid=5383163&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22028181%26dopt%3DAbstract</link>
            <description>CONCLUSIONSSeveral GK-MODY mutants show posttranslational defects in β-cells characterized by increased susceptibility to oxidative stress and/or protein instability. Regulation of GK activity through modulation of thiol status may be a physiological regulatory mechanism for the control of GK activity in β-cells.
    PMID: 22028181 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5383163</comments>
            <pubDate>Tue, 25 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5383163</guid>        </item>
        <item>
            <title>Stimulatory Effect of Insulin on Glucose Uptake by Muscle Involves the Central Nervous System in Insulin-Sensitive Mice.</title>
            <link>http://www.medworm.com/index.php?rid=5383162&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22028182%26dopt%3DAbstract</link>
            <description>CONCLUSIONSInsulin stimulates glucose uptake in muscle in part through effects via K(ATP) channels in the central nervous system, in analogy with the inhibitory effects of insulin on EGP. High-fat diet-induced obesity abolished the central effects of insulin on liver and muscle. These observations stress the role of central insulin resistance in the pathophysiology of diet-induced insulin resistance.
    PMID: 22028182 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5383162</comments>
            <pubDate>Tue, 25 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5383162</guid>        </item>
        <item>
            <title>Modulation of {beta}-Adrenergic Receptors in the Ventromedial Hypothalamus Influences Counterregulatory Responses to Hypoglycemia.</title>
            <link>http://www.medworm.com/index.php?rid=5383181&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22013013%26dopt%3DAbstract</link>
            <description>CONCLUSIONSLocal catecholamine release into the VMH enhances counterregulatory responses to hypoglycemia via stimulation of B2AR. These observations suggest that B2AR agonists might have therapeutic benefit in diabetic patients with defective glucose counterregulation.
    PMID: 22013013 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5383181</comments>
            <pubDate>Wed, 19 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5383181</guid>        </item>
        <item>
            <title>Elevated Glucose Represses Liver Glucokinase and Induces Its Regulatory Protein to Safeguard Hepatic Phosphate Homeostasis.</title>
            <link>http://www.medworm.com/index.php?rid=5383180&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22013014%26dopt%3DAbstract</link>
            <description>CONCLUSIONSThe lowering by glucose of the Gck-to-Gckr ratio provides a potential explanation for the impaired hepatic glucose uptake in diabetes. Elevated uric acid production at an elevated Gck -to-Gckr ratio supports a role for glucose regulation of gene expression in hepatic phosphate homeostasis.
    PMID: 22013014 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5383180</comments>
            <pubDate>Wed, 19 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5383180</guid>        </item>
        <item>
            <title>Convergence of the Insulin and Serotonin Programs in the Pancreatic {beta}-Cell.</title>
            <link>http://www.medworm.com/index.php?rid=5383178&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22013016%26dopt%3DAbstract</link>
            <description>CONCLUSIONSThese studies demonstrate that a common transcriptional cascade drives the differentiation of β-cells and serotonergic neurons and imparts the shared ability to produce serotonin. The interrelated biology of these two cell types has important implications for the pathology and treatment of diabetes.
    PMID: 22013016 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5383178</comments>
            <pubDate>Wed, 19 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5383178</guid>        </item>
        <item>
            <title>IL-21 Is an Antitolerogenic Cytokine of the Late-Phase Alloimmune Response.</title>
            <link>http://www.medworm.com/index.php?rid=5383177&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22013017%26dopt%3DAbstract</link>
            <description>CONCLUSIONSIL-21 interferes with different checkpoints of the FoxP3 Treg chain in the late phase of alloimmune response and, thus, acts as an antitolerogenic cytokine. Blockade of the IL-21/IL-21R pathway could be a precondition for tolerogenic protocols in transplantation.
    PMID: 22013017 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5383177</comments>
            <pubDate>Wed, 19 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5383177</guid>        </item>
        <item>
            <title>Control of Blood Glucose in the Absence of Hepatic Glucose Production During Prolonged Fasting in Mice: Induction of Renal and Intestinal Gluconeogenesis by Glucagon.</title>
            <link>http://www.medworm.com/index.php?rid=5383176&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22013018%26dopt%3DAbstract</link>
            <description>CONCLUSIONSOur study provides a definitive quantitative estimate of the capacity of extrahepatic gluconeogenesis to sustain fasting endogenous glucose production under the control of glucagon, regardless of the contribution of the liver. Thus, the current dogma relating to the respective role of the liver and of extrahepatic gluconeogenic organs in glucose homeostasis requires re-examination.
    PMID: 22013018 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5383176</comments>
            <pubDate>Wed, 19 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5383176</guid>        </item>
        <item>
            <title>Glucose-Dependent Insulinotropic Polypeptide: A Bifunctional Glucose-Dependent Regulator of Glucagon and Insulin Secretion in Humans.</title>
            <link>http://www.medworm.com/index.php?rid=5316768&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21984584%26dopt%3DAbstract</link>
            <description>CONCLUSIONSIn healthy subjects, GIP has no effect on glucagon responses during hyperglycemia while strongly potentiating insulin secretion. In contrast, GIP increases glucagon levels during fasting and hypoglycemic conditions, where it has little or no effect on insulin secretion. Thus, GIP seems to be a physiological bifunctional blood glucose stabilizer with diverging glucose-dependent effects on the two main pancreatic glucoregulatory hormones.
    PMID: 21984584 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5316768</comments>
            <pubDate>Thu, 13 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5316768</guid>        </item>
        <item>
            <title>Deficiency for Costimulatory Receptor 4-1BB Protects Against Obesity-Induced Inflammation and Metabolic Disorders.</title>
            <link>http://www.medworm.com/index.php?rid=5316767&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21998397%26dopt%3DAbstract</link>
            <description>CONCLUSIONSThese findings suggest that 4-1BB and 4-1BBL may be useful therapeutic targets for combating obesity-induced inflammation and metabolic disorders.
    PMID: 21998397 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5316767</comments>
            <pubDate>Thu, 13 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5316767</guid>        </item>
        <item>
            <title>Single Insulin-Specific CD8+ T Cells Show Characteristic Gene Expression Profiles in Human Type 1 Diabetes.</title>
            <link>http://www.medworm.com/index.php?rid=5316766&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21998398%26dopt%3DAbstract</link>
            <description>CONCLUSIONSPPI-specific CD8(+) T cells in type 1 diabetic patients include central memory and target different epitopes in new-onset versus long-standing disease. Our data support the hypothesis that insulin therapy may contribute to the expansion of autoreactive CD8(+) T cells in the long-term.
    PMID: 21998398 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5316766</comments>
            <pubDate>Thu, 13 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5316766</guid>        </item>
        <item>
            <title>WldS Enhances Insulin Transcription and Secretion via a SIRT1-Dependent Pathway and Improves Glucose Homeostasis.</title>
            <link>http://www.medworm.com/index.php?rid=5316765&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21998399%26dopt%3DAbstract</link>
            <description>DISCUSSIONOur results demonstrate that Wld(S) combines an insulinotropic effect with protection against β-cell failure and suggest that enhancing NAD biosynthesis in β-cells to increase SIRT1 activity could be a potential therapeutic approach for diabetes.
    PMID: 21998399 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5316765</comments>
            <pubDate>Thu, 13 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5316765</guid>        </item>
        <item>
            <title>The Effect of Rosiglitazone on Bone Quality in a Rat Model of Insulin Resistance and Osteoporosis.</title>
            <link>http://www.medworm.com/index.php?rid=5316764&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21998400%26dopt%3DAbstract</link>
            <description>CONCLUSIONSRSG decreases bone quality. An unusual finding was an increase in cortical bone porosity induced by RSG, consistent with its effect on long bones of women. ALN, an inhibitor of bone resorption, enhanced mechanical strength and may provide an approach to partially counter the deleterious skeletal effects of RSG.
    PMID: 21998400 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5316764</comments>
            <pubDate>Wed, 12 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5316764</guid>        </item>
        <item>
            <title>Islet Cholesterol Accumulation Due to Loss of ABCA1 Leads to Impaired Exocytosis of Insulin Granules.</title>
            <link>http://www.medworm.com/index.php?rid=5316763&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21998401%26dopt%3DAbstract</link>
            <description>CONCLUSIONSOur data highlight a crucial role of ABCA1 and cellular cholesterol in β-cells that is necessary for regulated insulin granule fusion events. These data suggest that abnormalities of cholesterol metabolism may contribute to the impaired β-cell function in diabetes.
    PMID: 21998401 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5316763</comments>
            <pubDate>Wed, 12 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5316763</guid>        </item>
        <item>
            <title>Impaired Expression of the Inducible cAMP Early Repressor Accounts for Sustained Adipose CREB Activity in Obesity.</title>
            <link>http://www.medworm.com/index.php?rid=5316762&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21998402%26dopt%3DAbstract</link>
            <description>CONCLUSIONSImpaired expression of ICER contributes to elevation in CREB target genes and, therefore, to the development of insulin resistance in obesity.
    PMID: 21998402 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5316762</comments>
            <pubDate>Wed, 12 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5316762</guid>        </item>
        <item>
            <title>PTPN2, a Candidate Gene for Type 1 Diabetes, Modulates Pancreatic {beta}-Cell Apoptosis via Regulation of the BH3-Only Protein Bim.</title>
            <link>http://www.medworm.com/index.php?rid=5316774&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21984578%26dopt%3DAbstract</link>
            <description>CONCLUSIONSThe present findings suggest that local IFN production may interact with a genetic factor (PTPN2) to induce aberrant proapoptotic activity of the BH3-only protein Bim, resulting in increased β-cell apoptosis via JNK activation and the intrinsic apoptotic pathway. This is the first indication of a direct interaction between a candidate gene for T1D and the activation of a specific downstream proapoptotic pathway in β-cells.
    PMID: 21984578 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5316774</comments>
            <pubDate>Fri, 07 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5316774</guid>        </item>
        <item>
            <title>{beta}-Cell Uncoupling Protein 2 Regulates Reactive Oxygen Species Production, Which Influences Both Insulin and Glucagon Secretion.</title>
            <link>http://www.medworm.com/index.php?rid=5316773&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21984579%26dopt%3DAbstract</link>
            <description>CONCLUSIONSUsing a novel β-cell-specific UCP2KO mouse model, we have shed light on UCP2 function in primary β-cells. UCP2 does not behave as a classical metabolic uncoupler in the β-cell, but has a more prominent role in the regulation of intracellular ROS levels that contribute to GSIS amplification. In addition, β-cell UCP2 contributes to the regulation of intraislet ROS signals that mediate changes in α-cell morphology and glucagon secretion.
    PMID: 21984579 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5316773</comments>
            <pubDate>Fri, 07 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5316773</guid>        </item>
        <item>
            <title>Decreased IRS2 and TIMP3 Expression in Monocytes From Offspring of Type 2 Diabetic Patients Is Correlated With Insulin Resistance and Increased Intima-Media Thickness.</title>
            <link>http://www.medworm.com/index.php?rid=5316772&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21984580%26dopt%3DAbstract</link>
            <description>CONCLUSIONSSystemic insulin resistance and subclinical atherosclerosis are associated with decreased IRS2 and TIMP3 expression in circulating monocytes.
    PMID: 21984580 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5316772</comments>
            <pubDate>Fri, 07 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5316772</guid>        </item>
        <item>
            <title>Early Treatment of NOD Mice With B7-H4 Reduces the Incidence of Autoimmune Diabetes.</title>
            <link>http://www.medworm.com/index.php?rid=5316771&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21984581%26dopt%3DAbstract</link>
            <description>CONCLUSIONSOur data demonstrate the protective role of B7-H4 in the development of autoimmune diabetes, suggesting a potential means of preventing type 1 diabetes by targeting the B7-H4 pathway.
    PMID: 21984581 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5316771</comments>
            <pubDate>Fri, 07 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5316771</guid>        </item>
        <item>
            <title>Brain Activation During Working Memory Is Altered in Type 1 Diabetes During Hypoglycemia.</title>
            <link>http://www.medworm.com/index.php?rid=5316770&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21984582%26dopt%3DAbstract</link>
            <description>CONCLUSIONSBOLD activation was increased and deactivation was decreased in type 1 diabetic versus control subjects during hypoglycemia. This higher level of brain activation required by type 1 diabetic subjects to attain the same level of cognitive performance as control subjects suggests reduced cerebral efficiency in type 1 diabetes.
    PMID: 21984582 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5316770</comments>
            <pubDate>Fri, 07 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5316770</guid>        </item>
        <item>
            <title>A Duodenal PKC-{delta} and Cholecystokinin Signaling Axis Regulates Glucose Production.</title>
            <link>http://www.medworm.com/index.php?rid=5316769&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21984583%26dopt%3DAbstract</link>
            <description>CONCLUSIONSIn summary, activation of duodenal PKC-δ leads to the stimulation of CCK release and activation of the CCK-A receptor signaling axis to lower glucose production in normal rats, but fails to bypass duodenal CCK-resistance in high fat-fed rats.
    PMID: 21984583 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5316769</comments>
            <pubDate>Fri, 07 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5316769</guid>        </item>
        <item>
            <title>Skeletal muscle triglycerides, diacylglycerols, and ceramides in insulin resistance: another paradox in endurance-trained athletes?</title>
            <link>http://www.medworm.com/index.php?rid=5283994&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21873552%26dopt%3DAbstract</link>
            <description>CONCLUSIONS Total myocellular DAGs were markedly higher in highly trained athletes, corresponding with higher insulin sensitivity, and suggest a more complex role for DAGs in insulin action. Our data also provide additional evidence in humans linking ceramides to insulin resistance. Finally, this study provides novel evidence supporting a role for specific skeletal muscle proteins involved in intramyocellular lipids, mitochondrial oxidative capacity, and insulin resistance.
    PMID: 21873552 [PubMed - in process] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5283994</comments>
            <pubDate>Sat, 01 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5283994</guid>        </item>
        <item>
            <title>Mechanisms of Control of the Free Ca2+ Concentration in the Endoplasmic Reticulum of Mouse Pancreatic {beta}-Cells: Interplay With Cell Metabolism and [Ca2+]c and Role of SERCA2b and SERCA3.</title>
            <link>http://www.medworm.com/index.php?rid=5283993&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21885870%26dopt%3DAbstract</link>
            <description>CONCLUSIONS [Ca(2+)](c) and [Ca(2+)](ER) oscillate in phase in response to glucose. Upon [Ca(2+)](c) increase, Ca(2+) is taken up by SERCA2b and SERCA3. Strong Ca(2+) influx triggers a Ca(2+) release from the ER that depends on SERCA3. SERCA3 deficiency neither impairs Ca(2+) uptake by the ER upon cell metabolism acceleration and insulin release nor induces ER stress.
    PMID: 21885870 [PubMed - in process] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5283993</comments>
            <pubDate>Sat, 01 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5283993</guid>        </item>
        <item>
            <title>Inhibition of id1 augments insulin secretion and protects against high-fat diet-induced glucose intolerance.</title>
            <link>http://www.medworm.com/index.php?rid=5283992&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21940780%26dopt%3DAbstract</link>
            <description>CONCLUSIONS These findings implicate Id1 as a negative regulator of insulin secretion. Id1 expression plays an essential role in the etiology of glucose intolerance, insulin secretory dysfunction, and β-cell dedifferentiation under conditions of increased lipid supply.
    PMID: 21940780 [PubMed - in process] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5283992</comments>
            <pubDate>Sat, 01 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5283992</guid>        </item>
        <item>
            <title>Fatty acids, obesity, and insulin resistance: time for a reevaluation.</title>
            <link>http://www.medworm.com/index.php?rid=5283991&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21948998%26dopt%3DAbstract</link>
            <description>Authors: Karpe F, Dickmann JR, Frayn KN
    PMID: 21948998 [PubMed - in process] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5283991</comments>
            <pubDate>Sat, 01 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5283991</guid>        </item>
        <item>
            <title>The complex mechanism of glutamate dehydrogenase in insulin secretion.</title>
            <link>http://www.medworm.com/index.php?rid=5283990&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21948999%26dopt%3DAbstract</link>
            <description>Authors: Fahien LA, Macdonald MJ
    PMID: 21948999 [PubMed - in process] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5283990</comments>
            <pubDate>Sat, 01 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5283990</guid>        </item>
        <item>
            <title>ID'ing a Novel Inhibitor of {beta}-Cell Function, Id1.</title>
            <link>http://www.medworm.com/index.php?rid=5283989&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21949000%26dopt%3DAbstract</link>
            <description>Authors: Billestrup N
    PMID: 21949000 [PubMed - in process] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5283989</comments>
            <pubDate>Sat, 01 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5283989</guid>        </item>
        <item>
            <title>Issues and events.</title>
            <link>http://www.medworm.com/index.php?rid=5283988&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21949001%26dopt%3DAbstract</link>
            <description>Authors: 
    PMID: 21949001 [PubMed - in process] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5283988</comments>
            <pubDate>Sat, 01 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5283988</guid>        </item>
        <item>
            <title>Prospectively Determined Impact of Type 1 Diabetes on Brain Volume During Development.</title>
            <link>http://www.medworm.com/index.php?rid=5283987&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21953611%26dopt%3DAbstract</link>
            <description>CONCLUSIONSThese results demonstrate that within diabetes, exposure to hyperglycemia and severe hypoglycemia may result in subtle deviation from normal developmental trajectories of the brain.
    PMID: 21953611 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5283987</comments>
            <pubDate>Tue, 27 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5283987</guid>        </item>
        <item>
            <title>Specific Control of Pancreatic Endocrine {beta}- and {delta}-Cell Mass by Class IIa Histone Deacetylases HDAC4, HDAC5, and HDAC9.</title>
            <link>http://www.medworm.com/index.php?rid=5283986&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21953612%26dopt%3DAbstract</link>
            <description>CONCLUSIONSWe conclude that HDAC4, -5, and -9 are key regulators to control the pancreatic β/δ-cell lineage. These results highlight the epigenetic mechanisms underlying the regulation of endocrine cell development and suggest new strategies for β-cell differentiation-based therapies.
    PMID: 21953612 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5283986</comments>
            <pubDate>Tue, 27 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5283986</guid>        </item>
        <item>
            <title>Specific Glucose-Induced Control of Insulin Receptor Substrate-2 Expression Is Mediated via Ca2+-Dependent Calcineurin/NFAT Signaling in Primary Pancreatic Islet {beta}-Cells.</title>
            <link>http://www.medworm.com/index.php?rid=5283997&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21940781%26dopt%3DAbstract</link>
            <description>CONCLUSIONSThe mechanism behind glucose-induced transcriptional control of IRS-2 gene expression specific to the islet β-cell is mediated by the Ca(2+)/calcineurin/NFAT pathway. This novel insight into the IRS-2 regulation could provide novel therapeutic means in type 2 diabetes to maintain an adequate functional mass.
    PMID: 21940781 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5283997</comments>
            <pubDate>Thu, 22 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5283997</guid>        </item>
        <item>
            <title>Forkhead Box O6 Integrates Insulin Signaling With Gluconeogenesis in the Liver.</title>
            <link>http://www.medworm.com/index.php?rid=5283996&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21940782%26dopt%3DAbstract</link>
            <description>CONCLUSIONSOur data uncover a FoxO6-dependent pathway by which the liver orchestrates insulin regulation of gluconeogenesis, providing the proof-of-concept that selective FoxO6 inhibition is beneficial for curbing excessive hepatic glucose production and improving glycemic control in diabetes.
    PMID: 21940782 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5283996</comments>
            <pubDate>Thu, 22 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5283996</guid>        </item>
        <item>
            <title>A Novel Cellular Defect in Diabetes: Membrane Repair Failure.</title>
            <link>http://www.medworm.com/index.php?rid=5283995&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21940783%26dopt%3DAbstract</link>
            <description>CONCLUSIONSBecause one consequence of repair failure is rapid cell death (via necrosis), our demonstration that repair fails in diabetes suggests a new mechanism by which myopathy develops in diabetes.
    PMID: 21940783 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5283995</comments>
            <pubDate>Thu, 22 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5283995</guid>        </item>
        <item>
            <title>Responses of Gut Microbiota and Glucose and Lipid Metabolism to Prebiotics in Genetic Obese and Diet-Induced Leptin-Resistant Mice.</title>
            <link>http://www.medworm.com/index.php?rid=5284001&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21933985%26dopt%3DAbstract</link>
            <description>CONCLUSIONSWe conclude that specific gut microbiota modulation improves glucose homeostasis, leptin sensitivity, and target enteroendocrine cell activity in obese and diabetic mice. By profiling the gut microbiota, we identified a catalog of putative bacterial targets that may affect host metabolism in obesity and diabetes.
    PMID: 21933985 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5284001</comments>
            <pubDate>Tue, 20 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5284001</guid>        </item>
        <item>
            <title>FoxO Feedback Control of Basal IRS-2 Expression in Pancreatic {beta}-Cells Is Distinct From That in Hepatocytes.</title>
            <link>http://www.medworm.com/index.php?rid=5284000&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21933986%26dopt%3DAbstract</link>
            <description>CONCLUSIONSThe molecular mechanism for feedback control of IRS signaling to decrease IRS-2 expression in liver and β-cells is quite distinct, with a predominant role played by FoxO3a in β-cells.
    PMID: 21933986 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5284000</comments>
            <pubDate>Tue, 20 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5284000</guid>        </item>
        <item>
            <title>TRB3 Gene Silencing Alleviates Diabetic Cardiomyopathy in a Type 2 Diabetic Rat Model.</title>
            <link>http://www.medworm.com/index.php?rid=5283999&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21933987%26dopt%3DAbstract</link>
            <description>Conclusions.TRB3 gene silencing may exert a protective effect on DCM by improving selective insulin resistance, implicating its potential role for treatment of human DCM.
    PMID: 21933987 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5283999</comments>
            <pubDate>Tue, 20 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5283999</guid>        </item>
        <item>
            <title>Abrogation of MMP-9 Gene Protects Against the Development of Retinopathy in Diabetic Mice by Preventing Mitochondrial Damage.</title>
            <link>http://www.medworm.com/index.php?rid=5283998&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21933988%26dopt%3DAbstract</link>
            <description>CONCLUSIONSRegulation of activated MMP-9 prevents retinal capillary cells from undergoing apoptosis by protecting mitochondrial ultrastructure and function and preventing mtDNA damage. Thus, MMP-9 inhibitors could have potential therapeutic value in preventing the development of diabetic retinopathy by preventing the continuation of the vicious cycle of mitochondrial damage.
    PMID: 21933988 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5283998</comments>
            <pubDate>Tue, 20 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5283998</guid>        </item>
        <item>
            <title>APPL1 Counteracts Obesity-Induced Vascular Insulin Resistance and Endothelial Dysfunction by Modulating the Endothelial Production of Nitric Oxide and Endothelin-1 in Mice.</title>
            <link>http://www.medworm.com/index.php?rid=5234800&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21926268%26dopt%3DAbstract</link>
            <description>CONCLUSIONSAPPL1 plays a key role in coordinating the vasodilator and vasoconstrictor effects of insulin by modulating Akt-dependent NO production and ERK1/2-mediated ET-1 secretion in the endothelium.
    PMID: 21926268 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5234800</comments>
            <pubDate>Fri, 16 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5234800</guid>        </item>
        <item>
            <title>Associations Between Paternally Transmitted Fetal IGF2 Variants and Maternal Circulating Glucose Concentrations in Pregnancy.</title>
            <link>http://www.medworm.com/index.php?rid=5234799&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21926269%26dopt%3DAbstract</link>
            <description>CONCLUSIONSPolymorphic variation in paternally transmitted fetal IGF2 is associated with increased maternal glucose concentrations in pregnancy and could potentially alter the risk of gestational diabetes in the mother. The association may be at least partially mediated by changes in placental IGF2 expression.
    PMID: 21926269 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5234799</comments>
            <pubDate>Fri, 16 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5234799</guid>        </item>
        <item>
            <title>Normal Glucagon Signaling and {beta}-Cell Function After Near-Total {alpha}-Cell Ablation in Adult Mice.</title>
            <link>http://www.medworm.com/index.php?rid=5234798&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21926270%26dopt%3DAbstract</link>
            <description>CONCLUSIONSAn extremely low amount of α-cells is sufficient to prevent a major counter-regulatory deregulation, both under physiologic and diabetic conditions. We previously reported that α-cells reprogram to insulin production after extreme β-cell loss and now conjecture that the low α-cell requirement could be exploited in future diabetic therapies aimed at regenerating β-cells by reprogramming adult α-cells.
    PMID: 21926270 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5234798</comments>
            <pubDate>Fri, 16 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5234798</guid>        </item>
        <item>
            <title>Loss of Intra-Islet CD20 Expression May Complicate Efficacy of B-Cell-Directed Type 1 Diabetes Therapies.</title>
            <link>http://www.medworm.com/index.php?rid=5234797&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21926271%26dopt%3DAbstract</link>
            <description>CONCLUSIONSThese findings provide important guidance for designing strategies targeting B cells as a potential means of diabetes intervention.
    PMID: 21926271 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5234797</comments>
            <pubDate>Fri, 16 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5234797</guid>        </item>
        <item>
            <title>High Resolution Magnetic Resonance Imaging Quantitatively Detects Individual Pancreatic Islets.</title>
            <link>http://www.medworm.com/index.php?rid=5234796&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21926272%26dopt%3DAbstract</link>
            <description>CONCLUSIONSData show that MEHFMRI quantitatively visualizes individual islets in the intact mouse pancreas, both ex vivo and in vivo.
    PMID: 21926272 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5234796</comments>
            <pubDate>Fri, 16 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5234796</guid>        </item>
        <item>
            <title>Non-Thyrotoxic Prevention of Diet-Induced Insulin Resistance by 3,5-Diiodo-L-Thyronine in Rats.</title>
            <link>http://www.medworm.com/index.php?rid=5234795&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21926273%26dopt%3DAbstract</link>
            <description>CONCLUSIONST2, by activating SIRT1, triggers a cascade of events resulting in improvement of the serum lipid profile, prevention of fat accumulation, and, finally, prevention of diet-induced insulin resistance.
    PMID: 21926273 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5234795</comments>
            <pubDate>Fri, 16 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5234795</guid>        </item>
        <item>
            <title>Fibroblast Growth Factor 21 (FGF21) in Human Cerebrospinal Fluid: Relationship With Plasma FGF21 and Body Adiposity.</title>
            <link>http://www.medworm.com/index.php?rid=5234794&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21926274%26dopt%3DAbstract</link>
            <description>CONCLUSIONSOur observations have important implications with respect to the potential central actions of FGF21. Future research should seek to clarify whether FGF21 would be beneficial in the management of obesity and its metabolic complications.
    PMID: 21926274 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5234794</comments>
            <pubDate>Fri, 16 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5234794</guid>        </item>
        <item>
            <title>Aberrant Accumulation of Undifferentiated Myeloid Cells in the Adipose Tissue of CCR2-Deficient Mice Delays Improvements in Insulin Sensitivity.</title>
            <link>http://www.medworm.com/index.php?rid=5234793&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21926275%26dopt%3DAbstract</link>
            <description>CONCLUSIONSThe discovery of this novel adipose tissue monocytic cell population provides advances toward understanding the pleiotropic role of CCR2 in monocyte/macrophage accumulation and regulation of adipose tissue inflammation.
    PMID: 21926275 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5234793</comments>
            <pubDate>Fri, 16 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5234793</guid>        </item>
        <item>
            <title>Arginase-2 Mediates Diabetic Renal Injury.</title>
            <link>http://www.medworm.com/index.php?rid=5234792&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21926276%26dopt%3DAbstract</link>
            <description>CONCLUSIONSThese findings indicate that arginase-2 plays a major role in induction of diabetic renal injury and that blocking arginase-2 activity or expression could be a novel therapeutic approach for treatment of DN.
    PMID: 21926276 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5234792</comments>
            <pubDate>Fri, 16 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5234792</guid>        </item>
        <item>
            <title>Vitamin D, Insulin Secretion, Sensitivity, and Lipids: Results From a Case-Control Study and a Randomized Controlled Trial Using Hyperglycemic Clamp Technique.</title>
            <link>http://www.medworm.com/index.php?rid=5221396&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21911741%26dopt%3DAbstract</link>
            <description>CONCLUSIONSVitamin D supplementation to apparently healthy subjects with insufficient serum 25(OH)D levels does not improve insulin sensitivity or secretion or serum lipid profile.
    PMID: 21911741 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5221396</comments>
            <pubDate>Mon, 12 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5221396</guid>        </item>
        <item>
            <title>Similar VLDL-TG Storage in Visceral and Subcutaneous Fat in Obese and Lean Women.</title>
            <link>http://www.medworm.com/index.php?rid=5221395&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21911742%26dopt%3DAbstract</link>
            <description>CONCLUSIONSVLDL-TG storage efficiency is similar in all regional fat depots, and trafficking of VLDL-TG into different adipose tissue depots was similar in UBO and lean women. Postabsorptive VLDL-TG storage is unlikely to be of major importance in the development of preferential upper-body fat distribution in obese women.
    PMID: 21911742 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5221395</comments>
            <pubDate>Mon, 12 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5221395</guid>        </item>
        <item>
            <title>Potential Role of Regulatory T Cells in Reversing Obesity-Linked Insulin Resistance and Diabetic Nephropathy.</title>
            <link>http://www.medworm.com/index.php?rid=5221394&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21911743%26dopt%3DAbstract</link>
            <description>CONCLUSIONSData suggest a potential therapeutic value of Tregs to improve insulin resistance and end organ damage in type 2 diabetes by limiting the proinflammatory milieu.
    PMID: 21911743 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5221394</comments>
            <pubDate>Mon, 12 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5221394</guid>        </item>
        <item>
            <title>Activation of Protein Kinase C-{zeta} in Pancreatic {beta}-Cells In Vivo Improves Glucose Tolerance and Induces {beta}-Cell Expansion via mTOR Activation.</title>
            <link>http://www.medworm.com/index.php?rid=5221393&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21911744%26dopt%3DAbstract</link>
            <description>CONCLUSIONSPKC-ζ, through mTOR activation, modifies the expression pattern of β-cell cycle molecules leading to increased β-cell replication and mass with a concomitant enhancement in β-cell function. Approaches to enhance PKC-ζ activity may be of value as a therapeutic strategy for the treatment of diabetes.
    PMID: 21911744 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5221393</comments>
            <pubDate>Mon, 12 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5221393</guid>        </item>
        <item>
            <title>Advanced Glycation End Products Are Direct Modulators of {beta}-Cell Function.</title>
            <link>http://www.medworm.com/index.php?rid=5221392&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21911745%26dopt%3DAbstract</link>
            <description>CONCLUSIONSThese findings demonstrate that AGEs directly cause insulin secretory defects, most likely by impairing mitochondrial function, which may contribute to the development of T1D.
    PMID: 21911745 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5221392</comments>
            <pubDate>Mon, 12 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5221392</guid>        </item>
        <item>
            <title>Effects of Genetic Susceptibility for Type 2 Diabetes on the Evolution of Glucose Homeostasis Traits Before and After Diabetes Diagnosis: Data From the D.E.S.I.R. Study.</title>
            <link>http://www.medworm.com/index.php?rid=5221391&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21911746%26dopt%3DAbstract</link>
            <description>CONCLUSIONSAfter incident T2D, TCF7L2 at-risk variants were associated with a faster decrease in β-cell function compared with those with the CC genotype. There was a joint effect of family history of T2D and TCF7L2 risk variant on the rise in glycemia and the decrease in insulin secretion at the end of follow-up, suggesting the joint influence of the combination of diabetes genetic predisposition with familial factors on the evolution of glycemia over time.
    PMID: 21911746 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5221391</comments>
            <pubDate>Mon, 12 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5221391</guid>        </item>
        <item>
            <title>Inflammation Is Necessary for Long-Term but Not Short-Term High-Fat Diet-Induced Insulin Resistance.</title>
            <link>http://www.medworm.com/index.php?rid=5221390&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21911747%26dopt%3DAbstract</link>
            <description>CONCLUSIONSThese data suggest that the initial stage of HFD-induced insulin resistance is independent of inflammation, whereas the more chronic state of insulin resistance in established obesity is largely mediated by macrophage-induced proinflammatory actions. The early onset insulin resistance during HFD feeding is more likely related to acute tissue lipid overload.
    PMID: 21911747 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5221390</comments>
            <pubDate>Mon, 12 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5221390</guid>        </item>
        <item>
            <title>Intervention With an Erythropoietin-Derived Peptide Protects Against Neuroglial and Vascular Degeneration During Diabetic Retinopathy.</title>
            <link>http://www.medworm.com/index.php?rid=5221389&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21911748%26dopt%3DAbstract</link>
            <description>CONCLUSIONSTreatment with an EPO-derived peptide after diabetes is fully established can significantly protect against neuroglial and vascular degenerative pathology without altering hematocrit or exacerbating neovascularization. These findings have therapeutic implications for disorders such as diabetic retinopathy.
    PMID: 21911748 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5221389</comments>
            <pubDate>Mon, 12 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5221389</guid>        </item>
        <item>
            <title>CPVL/CHN2 Genetic Variant Is Associated With Diabetic Retinopathy in Chinese Type 2 Diabetic Patients.</title>
            <link>http://www.medworm.com/index.php?rid=5221388&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21911749%26dopt%3DAbstract</link>
            <description>CONCLUSIONSIn this study, we found CPVL/CHN2 rs39059 was associated with diabetic retinopathy in the Chinese type 2 diabetic patients.
    PMID: 21911749 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5221388</comments>
            <pubDate>Mon, 12 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5221388</guid>        </item>
        <item>
            <title>Elevated NF-{kappa}B Activation Is Conserved in Human Myocytes Cultured From Obese Type 2 Diabetic Patients and Attenuated by AMP-Activated Protein Kinase.</title>
            <link>http://www.medworm.com/index.php?rid=5221387&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21911750%26dopt%3DAbstract</link>
            <description>CONCLUSIONSThis work provides solid evidence that differentiated human muscle precursor cells maintain in vivo phenotypes of inflammation and insulin resistance and that obesity alone may not be sufficient to establish inflammation in these cells. It is important that we demonstrate an anti-inflammatory role for AMPK in these human cells. Despite attenuation of NF-κB activity by AMPK, insulin resistance in obese T2D cells remained, suggesting factors in addition to inflammation may contribute to the insulin resistance phenotype in muscle cells.
    PMID: 21911750 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5221387</comments>
            <pubDate>Mon, 12 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5221387</guid>        </item>
        <item>
            <title>Endothelial NO/cGMP/VASP Signaling Attenuates Kupffer Cell Activation and Hepatic Insulin Resistance Induced by High-Fat Feeding.</title>
            <link>http://www.medworm.com/index.php?rid=5221386&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21911751%26dopt%3DAbstract</link>
            <description>CONCLUSIONSThese results collectively imply a physiological role for endothelial NO to limit obesity-associated inflammation and insulin resistance in hepatocytes and support a model in which Kupffer cell activation during high-fat feeding is dependent on reduced NO signaling. Our findings also identify the NO/VASP pathway as a novel potential target for the treatment of obesity-associated liver insulin resistance.
    PMID: 21911751 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5221386</comments>
            <pubDate>Mon, 12 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5221386</guid>        </item>
        <item>
            <title>Prospective Associations of Vitamin D With {beta}-Cell Function and Glycemia: The Prospective Metabolism and Islet Cell Evaluation (PROMISE) Cohort Study.</title>
            <link>http://www.medworm.com/index.php?rid=5221385&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21911752%26dopt%3DAbstract</link>
            <description>CONCLUSIONSHigher baseline 25(OH)D independently predicted better β-cell function and lower AUC(glucose) at follow-up, supporting a potential role for vitamin D in type 2 diabetes etiology.
    PMID: 21911752 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5221385</comments>
            <pubDate>Mon, 12 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5221385</guid>        </item>
        <item>
            <title>Increased Phagocyte-Like NADPH Oxidase and Reactive Oxygen Species Generation in Type 2 Diabetic ZDF Rat and Human Islets: Role of Rac1-Jun NH2-Terminal Kinase 1/2 Signaling Pathway in Mitochondrial Dysregulation in the Diabetic Islet.</title>
            <link>http://www.medworm.com/index.php?rid=5221384&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21911753%26dopt%3DAbstract</link>
            <description>CONCLUSIONSWe provide the first in vitro and in vivo evidence in support of an accelerated Rac1-Nox-ROS-JNK1/2 signaling pathway in the islet β-cell leading to the onset of mitochondrial dysregulation in diabetes.
    PMID: 21911753 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5221384</comments>
            <pubDate>Mon, 12 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5221384</guid>        </item>
        <item>
            <title>Targeted Inhibition of Calpain Reduces Myocardial Hypertrophy and Fibrosis in Mouse Models of Type 1 Diabetes.</title>
            <link>http://www.medworm.com/index.php?rid=5221383&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21911754%26dopt%3DAbstract</link>
            <description>CONCLUSIONSMyocardial hypertrophy and fibrosis in diabetic mice are attenuated by reduction of calpain function. Thus targeted inhibition of calpain represents a potential novel therapeutic strategy for reversing diabetic cardiomyopathy.
    PMID: 21911754 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5221383</comments>
            <pubDate>Mon, 12 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5221383</guid>        </item>
        <item>
            <title>C-Peptide Response and HLA Genotypes in Subjects With Recent-Onset Type 1 Diabetes After Immunotherapy With DiaPep277: An Exploratory Study.</title>
            <link>http://www.medworm.com/index.php?rid=5221403&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21896927%26dopt%3DAbstract</link>
            <description>CONCLUSIONSThis exploratory study demonstrates that type 1 diabetic adults with low and moderate risk HLA genotypes benefit the most from intervention with DiaPep277; the only subgroup with an increase of C-peptide at 12 months after diagnosis was the low risk DiaPep277-treated subgroup.
    PMID: 21896927 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5221403</comments>
            <pubDate>Tue, 06 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5221403</guid>        </item>
        <item>
            <title>Mediobasal Hypothalamic Sirtuin 1 Is Essential for Resveratrol's Effects on Insulin Action in Rats.</title>
            <link>http://www.medworm.com/index.php?rid=5221402&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21896928%26dopt%3DAbstract</link>
            <description>CONCLUSIONSTaken together, these studies demonstrate that resveratrol improves glucose homeostasis mainly through a central SIRT1-dependent pathway and that the MBH is a major site of resveratrol action.
    PMID: 21896928 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5221402</comments>
            <pubDate>Tue, 06 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5221402</guid>        </item>
        <item>
            <title>Role of Lipid Peroxidation and PPAR-{delta} in Amplifying Glucose-Stimulated Insulin Secretion.</title>
            <link>http://www.medworm.com/index.php?rid=5221401&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21896929%26dopt%3DAbstract</link>
            <description>CONCLUSIONSElevated glucose levels augment the release of AA and LA from phospholipids and their peroxidation to 4-HNE in β-cells. This molecule is an endogenous ligand for PPAR-δ, which amplifies insulin secretion in β-cells.
    PMID: 21896929 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5221401</comments>
            <pubDate>Tue, 06 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5221401</guid>        </item>
        <item>
            <title>Deletion of the G6pc2 Gene Encoding the Islet-Specific Glucose-6-Phosphatase Catalytic Subunit-Related Protein Does Not Affect the Progression or Incidence of Type 1 Diabetes in NOD/ShiLtJ Mice.</title>
            <link>http://www.medworm.com/index.php?rid=5221400&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21896930%26dopt%3DAbstract</link>
            <description>CONCLUSIONSThese results demonstrate that G6pc2 is an important driver for the selection and expansion of islet-reactive CD8(+) T cells infiltrating NOD/ShiLtJ islets. However, autoreactivity to G6pc2 is not essential for the emergence of autoimmune diabetes. The results remain consistent with previous studies indicating that insulin may be the primary autoimmune target, at least in NOD/ShiLtJ mice.
    PMID: 21896930 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5221400</comments>
            <pubDate>Tue, 06 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5221400</guid>        </item>
        <item>
            <title>Angiotensin II Receptors Modulate Muscle Microvascular and Metabolic Responses to Insulin In Vivo.</title>
            <link>http://www.medworm.com/index.php?rid=5221399&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21896931%26dopt%3DAbstract</link>
            <description>CONCLUSIONSWe conclude that both AT(1)Rs and AT(2)Rs regulate insulin's microvascular and metabolic action in muscle. Although AT(1)R activity restrains muscle metabolic responses to insulin via decreased microvascular recruitment and insulin delivery, AT(2)R activity is required for normal microvascular responses to insulin. Thus, pharmacologic manipulation aimed at increasing the AT(2)R-to-AT(1)R activity ratio may afford the potential to improve muscle insulin sensitivity and glucose metabolism.
    PMID: 21896931 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5221399</comments>
            <pubDate>Tue, 06 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5221399</guid>        </item>
        <item>
            <title>Expansion of Th17 Cells and Functional Defects in T Regulatory Cells Are Key Features of the Pancreatic Lymph Nodes in Patients With Type 1 Diabetes.</title>
            <link>http://www.medworm.com/index.php?rid=5221398&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21896932%26dopt%3DAbstract</link>
            <description>CONCLUSIONSThese data provide evidence for an unbalanced immune status in the PLNs of type 1 diabetic subjects, and treatments restoring the immune homeostasis in the target organ of these patients represent a potential therapeutic strategy.
    PMID: 21896932 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5221398</comments>
            <pubDate>Tue, 06 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5221398</guid>        </item>
        <item>
            <title>Genetic Examination of SETD7 and SUV39H1/H2 Methyltransferases and the Risk of Diabetes Complications in Patients With Type 1 Diabetes.</title>
            <link>http://www.medworm.com/index.php?rid=5221397&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21896933%26dopt%3DAbstract</link>
            <description>CONCLUSIONSOur findings propose that a genetic variation in a gene coding for a histone methyltransferase is protective for a diabetic microvascular complication. The pathophysiological implications of this polymorphism or other genetic variation nearby for the vascular complications of type 1 diabetes remain to be investigated.
    PMID: 21896933 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5221397</comments>
            <pubDate>Tue, 06 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5221397</guid>        </item>
        <item>
            <title>Targeting Curcusomes to Inflammatory Dendritic Cells Inhibits NF-{kappa}B and Improves Insulin Resistance in Obese Mice.</title>
            <link>http://www.medworm.com/index.php?rid=5195503&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21885868%26dopt%3DAbstract</link>
            <description>CONCLUSIONSBoth hepatic Tip-DCs and ATMs contribute to insulin resistance in ob/ob mice. Curcusome nanoparticles inhibit proinflammatory pathways in hepatic Tip-DCs and ATMs and reverse insulin resistance. Targeting inflammatory DCs is a novel approach for type 2 diabetes treatment.
    PMID: 21885868 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5195503</comments>
            <pubDate>Wed, 31 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5195503</guid>        </item>
        <item>
            <title>CCK Stimulation of GLP-1 Neurons Involves {alpha}1-Adrenoceptor-Mediated Increase in Glutamatergic Synaptic Inputs.</title>
            <link>http://www.medworm.com/index.php?rid=5195502&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21885869%26dopt%3DAbstract</link>
            <description>CONCLUSIONSCCK activates NTS-PPG cells by a circuit involving adrenergic and glutamatergic neurones. NTS-PPG neurons integrate a variety of peripheral signals that indicate both long-term energy balance and short-term nutritional and digestional status to produce an output signal to feeding and autonomic circuits.
    PMID: 21885869 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5195502</comments>
            <pubDate>Wed, 31 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5195502</guid>        </item>
        <item>
            <title>Mechanisms of Control of the Free Ca2+ Concentration in the Endoplasmic Reticulum of Mouse Pancreatic {beta}-Cells: Interplay With Cell Metabolism and [Ca2+]c, and Role of SERCA2b and SERCA3.</title>
            <link>http://www.medworm.com/index.php?rid=5195501&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21885870%26dopt%3DAbstract</link>
            <description>CONCLUSIONS[Ca(2+)](c) and [Ca(2+)](ER) oscillate in phase in response to glucose. Upon [Ca(2+)](c) increase, Ca(2+) is taken up by SERCA2b and SERCA3. Strong Ca(2+) influx triggers a Ca(2+) release from the ER that depends on SERCA3. SERCA3 deficiency neither impairs Ca(2+) uptake by the ER upon cell metabolism acceleration and insulin release nor induces ER stress.
    PMID: 21885870 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5195501</comments>
            <pubDate>Wed, 31 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5195501</guid>        </item>
        <item>
            <title>miR-146a-Mediated Extracellular Matrix Protein Production in Chronic Diabetes Complications.</title>
            <link>http://www.medworm.com/index.php?rid=5195500&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21885871%26dopt%3DAbstract</link>
            <description>CONCLUSIONSThese studies showed a novel, glucose-induced molecular mechanism in which miR-146a participates in the transcriptional circuitry regulating extracellular matrix protein production in diabetes.
    PMID: 21885871 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5195500</comments>
            <pubDate>Wed, 31 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5195500</guid>        </item>
        <item>
            <title>Hepatic Glucagon Action Is Essential for Exercise-Induced Reversal of Mouse Fatty Liver.</title>
            <link>http://www.medworm.com/index.php?rid=5195499&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21885872%26dopt%3DAbstract</link>
            <description>CONCLUSIONSThese findings suggest that therapies that use antagonism of hepatic glucagon action to reduce blood glucose may interfere with the ability of exercise and perhaps other interventions to positively affect fatty liver.
    PMID: 21885872 [PubMed - as supplied by publisher] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5195499</comments>
            <pubDate>Wed, 31 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5195499</guid>        </item>
        <item>
            <title>Comment on: Hoeg et al. Lipid-Induced Insulin Resistance Affects Women Less Than Men and Is Not Accompanied by Inflammation or Impaired Proximal Insulin Signaling. Diabetes 2011;60:64-73.</title>
            <link>http://www.medworm.com/index.php?rid=5180243&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21868787%26dopt%3DAbstract</link>
            <description>Authors: Cusi K
    PMID: 21868787 [PubMed - in process] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5180243</comments>
            <pubDate>Wed, 31 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5180243</guid>        </item>
        <item>
            <title>Response to Comment on: Hoeg et al. Lipid-Induced Insulin Resistance Affects Women Less Than Men and Is Not Accompanied by Inflammation or Impaired Proximal Insulin Signaling. Diabetes 2011;60:64-73.</title>
            <link>http://www.medworm.com/index.php?rid=5180242&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21868788%26dopt%3DAbstract</link>
            <description>Authors: Kiens B, Høeg LD, Sjøberg KA
    PMID: 21868788 [PubMed - in process] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5180242</comments>
            <pubDate>Wed, 31 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5180242</guid>        </item>
        <item>
            <title>Comment on: Berhan. Thirty Years of Prospective Nationwide Incidence of Childhood Type 1 Diabetes: The Accelerating Increase by Time Tends to Level Off in Sweden. Diabetes 2011;60:577-581.</title>
            <link>http://www.medworm.com/index.php?rid=5180241&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21868789%26dopt%3DAbstract</link>
            <description>Authors: Howard SG
    PMID: 21868789 [PubMed - in process] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5180241</comments>
            <pubDate>Wed, 31 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5180241</guid>        </item>
        <item>
            <title>Postprandial insulin secretion after gastric bypass surgery: the role of glucagon-like Peptide 1.</title>
            <link>http://www.medworm.com/index.php?rid=5180240&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21868790%26dopt%3DAbstract</link>
            <description>Authors: Holst JJ
    PMID: 21868790 [PubMed - in process] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5180240</comments>
            <pubDate>Wed, 31 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5180240</guid>        </item>
        <item>
            <title>Gastric bypass surgery enhances glucagon-like Peptide 1-stimulated postprandial insulin secretion in humans.</title>
            <link>http://www.medworm.com/index.php?rid=5180239&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21868791%26dopt%3DAbstract</link>
            <description>CONCLUSIONS Increased GLP-1-stimulated insulin secretion contributes significantly to hyperinsulinism in GB subjects. However, the exaggerated effect of GLP-1 on postprandial insulin secretion in surgical subjects is not significantly different in those with and without recurrent hypoglycemia.
    PMID: 21868791 [PubMed - in process] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5180239</comments>
            <pubDate>Wed, 31 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5180239</guid>        </item>
        <item>
            <title>Issues and events.</title>
            <link>http://www.medworm.com/index.php?rid=5180238&amp;cid=s_37676_15_f&amp;fid=37676&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21868792%26dopt%3DAbstract</link>
            <description>Authors: 
    PMID: 21868792 [PubMed - in process] (Source: Diabetes)</description>
            <author>Diabetes</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5180238</comments>
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