肥胖相关性胰岛素抵抗发生机制

被引:38
作者
余鹏
袁刚
机构
[1] 华中科技大学同济医学院附属同济医院内分泌科
关键词
肥胖; 胰岛素抵抗; 游离脂肪酸; 炎性因子; 线粒体功能障碍; 内质网应激;
D O I
10.13730/j.issn.1009-2595.2017.03.019
中图分类号
R587.1 [糖尿病]; R589.7 [嘌呤(Purine)代谢障碍];
学科分类号
100201 [内科学];
摘要
<正>胰岛素抵抗(insulin resistance,IR)是指胰岛素在其靶器官的生物学作用降低,在分子水平上表现为胰岛素信号通路受损。肥胖是导致IR的重要原因,但肥胖导致IR的分子机制并未完全明确。有研究提示,肥胖所导致的脂质代谢紊乱、炎性因子分泌增加,以及肥胖状态下出现的胰岛素靶细胞线粒体功能障碍、氧化应激、内质网应激等在IR的发生、发展中起到了一定的作用,本文就这些机制做一综述。1游离脂肪酸(free fatty acid,FFA)与IR FFA是组织器官的能源物质,细胞内FFA可用
引用
收藏
页码:213 / 217
页数:5
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