...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>The FASEB Journal >Deletion of diacylglycerol kinase epsilon confers susceptibility to obesity via reduced lipolytic activity in murine adipocytes
【24h】

Deletion of diacylglycerol kinase epsilon confers susceptibility to obesity via reduced lipolytic activity in murine adipocytes

机译：Deletion of diacylglycerol kinase epsilon confers susceptibility to obesity via reduced lipolytic activity in murine adipocytes

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

摘要

Lipid metabolism is closely involved with signal transduction and energy homeostasis. Excess calorie intake causes abnormal lipid metabolism, promoting obesity and insulin resistance. Diacylglycerol (DG) represents not only a lipidic second messenger but also an intermediate metabolite for triglyceride metabolism in the endoplasmic reticulum (ER). However, it remains undetermined how the roles of DG in signaling and energy homeostasis is regulated within the cell. Of DG kinases (DGKs), which are enzymes that phosphorylate DG, DGK epsilon resides in the ER. This study examined how DGK epsilon is implicated in signal transduction and lipid homeostasis. DGK epsilon-deficient mice were fed a high-fat diet (HFD) for 40 d. We observed that DGK epsilon deficiency promotes fat accumulation in adipocytes and subsequently promotes insulin resistance in mice fed an HFD. This abnormal fat metabolism is mediated by down-regulation of lipolytic activities, such as adipose triglyceride lipase and hormone-sensitive lipase. In addition, activation of DG-sensitive PKC leads to insulin resistance in adipose tissue, which may be caused by delayed metabolism of DG. Our data suggest that DGK epsilon links the second messenger signaling system to energy homeostasis in adipocytes and that its deficiency results in abnormal lipid metabolism such as obesity and insulin resistance.Nakano, T., Seino, K., Wakabayashi, I., Stafforini, D. M., Topham, M. K., Goto, K. Deletion of diacylglycerol kinase epsilon confers susceptibility to obesity via reduced lipolytic activity in murine adipocytes.

著录项

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