The UPS in diabetes and obesity.
The UPS in diabetes and obesity.
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糖尿病和肥胖症中的UPS。
DOI：
10.1186/1471-2091-9-s1-s6
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发表时间：
2008-10-21
期刊：
影响因子：
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通讯作者：
Wing, Simon S.
中科院分区：
文献类型：
--
作者：
Wing, Simon S.
2型糖尿病是由胰岛素信号传导和胰岛素分泌缺陷引起的。虽然泛素蛋白酶体系统（UPS）在2型糖尿病发病机制中的作用在很大程度上仍未被探索，但文献中的一些例子是有趣的，并为药物开发提供了靶点。研究表明，胰岛素抵抗可以通过刺激胰岛素信号通路中的重要分子，特别是胰岛素受体底物蛋白IRS1、IRS2和激酶AKT1（Akt）的降解来诱导。此外，由于胰腺β细胞中UPS介导的IRS2降解，可能发生胰岛素分泌缺陷。UPS似乎还参与调节脂肪细胞中的脂质合成和肝脏的脂质产生，并可能影响肥胖的发展。诱导胰岛素信号传导和分泌缺陷的其他可能机制仍有待探索，包括泛素化在胰岛素受体内化和运输中的作用。从Current BioData的靶向蛋白质数据库（TPdb;）重新发布。
Type 2 diabetes is caused by defects in both insulin signaling and insulin secretion. Though the role of the ubiquitin proteasome system (UPS) in the pathogenesis of type 2 diabetes remains largely unexplored, the few examples present in the literature are interesting and suggest targets for drug development. Studies indicate that insulin resistance can be induced by stimulating the degradation of important molecules in the insulin signaling pathway, in particular the insulin receptor substrate proteins IRS1, IRS2 and the kinase AKT1 (Akt). In addition, a defect in insulin secretion could occur due to UPS-mediated degradation of IRS2 in the β-cells of the pancreas. The UPS also appears to be involved in regulating lipid synthesis in adipocytes and lipid production by the liver and could influence the development of obesity. Other possible mechanisms for inducing defects in insulin signaling and secretion remain to be explored, including the role of ubiquitylation in insulin receptor internalization and trafficking. Republished from Current BioData's Targeted Proteins database (TPdb; ).