基础医学与临床 ›› 2008, Vol. 28 ›› Issue (8): 886-889.

• 短篇综述 • 上一篇    下一篇

氧化应激与2型糖尿病

王方 孟雁   

  1. 基础医学研究所
  • 收稿日期:2007-09-04 修回日期:2001-09-17 出版日期:2008-08-25 发布日期:2008-08-25

Oxidative stress and type 2 diabetes

Fang WANG, Yan MENG   

  1. Institute of Basic Medical Sciences,CAMS & PUMC
  • Received:2007-09-04 Revised:2001-09-17 Online:2008-08-25 Published:2008-08-25

摘要: 胰岛素抵抗、胰岛 细胞功能受损是2型糖尿病的主要病因。高血糖、高血脂导致在代谢过程中,线粒体产生大量活性氧,其可损坏线粒体功能,引起氧化应激反应。氧化应激可以产生以下结果:(1)阻断胰岛素作用通路,导致胰岛素抵抗;(2)降低胰岛素基因表达水平;(3)抑制胰岛素分泌;(4)促进 细胞凋亡等。本文主要针对活性氧的产生、氧化应激诱导胰岛素抵抗和胰岛 细胞功能受损等机制进行了综述。

Abstract: Insulin resistance and islet cell dysfunction are the main pathogenesis of type 2 diabetes. The generation of a great quantity of mitochondrial reactive oxygen species (ROS) impairs the function of mitochondria and induces oxidative stress during metabolic process of hyperglycaemia and hyperlipemia. Oxidative stress results in: (1) block the insulin action pathway and induce insulin resistance; (2) depress the expression of insulin gene; (3) decrease insulin secretion; (4) impair cell function. In this paper, we summary the mechanism of the ROS generation, insulin resistance and cell dysfunction induced by oxidative stress.