机译:核孤儿受体TAK1 / TR4缺陷小鼠受到保护,防止肥胖相关的炎症,肝脂肪变性和胰岛素抵抗
Hong Soon Kang,1 Kyoko Okamoto,1 Yong-Sik Kim,1 Yukimasa Takeda,1 Carl D. Bortner,2 Huaixin Dang,1 Taira Wada,3 Wen Xie,3 Xiao-Ping Yang,1 Grace Liao/ and Anton M. Jetten1From the 1 Cell Biology Section, Laboratory of Respiratory Biology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, the 2 Laboratory of Signal Transduction, Division of Intramural Research, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, and the ''Center for Pharmacogenetics and Department of Pharmaceutical Sciences, University of Pittsburgh, Pittsburgh, Pennsylvania.Corresponding author: Anton M. Jetten, jetten@niehs.nih.gov.Received 4 May 2010 and accepted 14 September 2010. Published ahead of print at http,//diabetes.diabetesjournals.org on 23 September 2010. DOI: 10.2337/dbl0-0628.© 2011 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenseS/by-nc-nd/3.0/ for details.The costs of publication of this article were defrayed in part, by ifie payment, of page chtuyes. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.,;
机译:核孤儿受体TAK1 / TR4缺陷小鼠受到保护,防止肥胖相关的炎症,肝脂肪变性和胰岛素抵抗
机译:肝脏巨噬细胞的维生素D受体激活改善了小鼠肝脏炎症,脂肪变性和胰岛素抵抗力
机译:低密度脂蛋白受体相关蛋白1保护免受肝胰岛素抵抗和肝脂肪变性。
机译:孤儿核受体的激动剂:动物模型中培养细胞和HDL水平的诱导eAPO e合成之间的关系
机译:脂蛋白受体SR-B1缺乏增强脂肪组织炎症,并在小鼠饮食诱导的肥胖期间减少对肝脏脂肪变性的易感性
机译:核孤儿受体TAK1 / TR4缺陷小鼠受到保护防止肥胖相关的炎症肝脂肪变性和胰岛素抵抗
机译:核孤儿受体TAK1 / TR4缺陷小鼠受到保护,以防止肥胖相关的炎症,肝脂肪变性和胰岛素抵抗