...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Journal of Lipid Research >G0/G1 switch gene-2 regulates human adipocyte lipolysis by affecting activity and localization of adipose triglyceride lipase
【24h】

G0/G1 switch gene-2 regulates human adipocyte lipolysis by affecting activity and localization of adipose triglyceride lipase

机译：G0 / G1开关基因-2通过影响脂肪甘油三酯脂酶的活性和定位来调节人脂肪细胞的脂解作用

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

The hydrolysis of triglycerides in adipocytes, termed lipolysis, provides free fatty acids as energy fuel. Murine lipolysis largely depends on the activity of adipose triglyceride lipase (ATGL), which is regulated by two proteins annotated as comparative gene identification-58 (CGI-58) and G0/G1 switch gene-2 (G0S2). CGI-58 activates and G0S2 inhibits ATGL activity. In contrast to mice, the functional role of G0S2 in human adipocyte lipolysis is poorly characterized. Here we show that overexpression or silencing of G0S2 in human SGBS adipocytes decreases and increases lipolysis, respectively. Human G0S2 is upregulated during adipocyte differentiation and inhibits ATGL activity in a dose-dependent manner. Interestingly, C-terminally truncated ATGL mutants, which fail to localize to lipid droplets, translocate to the lipid droplet upon coexpression with G0S2, suggesting that G0S2 anchors ATGL to lipid droplets independent of ATGL's C-terminal lipid binding domain. Taken together, our results indicate that G0S2 also regulates human lipolysis by affecting enzyme activity and intracellular localization of ATGL. Increased lipolysis is known to contribute to the pathogenesis of insulin resistance, and G0S2 expression has been shown to be reduced in poorly controlled type 2 diabetic patients. Our data indicate that downregulation of G0S2 in adipose tissue could represent one of the underlying causes leading to increased lipolysis in the insulin-resistant state.
机译：脂肪细胞中甘油三酸酯的水解（称为脂解）可提供游离脂肪酸作为能源。鼠脂解很大程度上取决于脂肪甘油三酸酯脂肪酶（ATGL）的活性，该活性受两种蛋白质的调节，分别标记为比较基因识别-58（CGI-58）和G0 / G1转换基因2（G0S2）。 CGI-58激活，而G0S2抑制ATGL活性。与小鼠相比，G0S2在人脂肪细胞脂解中的功能作用较差。在这里，我们显示人类SGBS脂肪细胞中G0S2的过表达或沉默分别降低和增加了脂解作用。人G0S2在脂肪细胞分化期间被上调，并以剂量​​依赖性方式抑制ATGL活性。有趣的是，未能定位于脂质小滴的C末端截短的ATGL突变体在与G0S2共表达时易位至脂质小滴，表明G0S2将ATGL锚定于独立于ATGL的C末端脂质结合域的脂质小滴。两者合计，我们的结果表明，G0S2还通过影响酶活性和ATGL的细胞内定位来调节人的脂解作用。已知增加的脂解作用可导致胰岛素抵抗，并且在控制不佳的2型糖尿病患者中，GOS2的表达降低。我们的数据表明，脂肪组织中G0S2的下调可能是导致胰岛素抵抗状态下脂解增加的根本原因之一。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号