胰岛β细胞葡萄糖毒性分子机制的研究进展  

Advances in molecular mechanisms of pancreatic beta-cell glucotoxicity

作　　者：张珊珊[1] 吴木潮[1] 

机构地区：[1]中山大学孙逸仙纪念医院内分泌科,广州510120

出　　处：《国际医药卫生导报》2013年第9期1381-1384,共4页International Medicine and Health Guidance News

摘　　要：慢性高糖可损伤胰岛β细胞，这被称为“葡萄糖毒性”。胰岛β细胞葡萄糖毒性涉及多种机制包括氧化应激、内质网应激、线粒体功能失调、炎症、糖基化终末产物形成、低氧状态与低氧诱导因子激活、胰岛β细胞分化表型丧失，等等。目前认为，氧化应激、内质网应激和胰岛β细胞分化表型的丧失在胰岛β细胞葡萄糖毒性中的作用较为明确；其中氧化应激在糖尿病胰岛β细胞葡萄糖毒性中发挥中心性作用。The deterioration of beta-cell function and survival caused by chronic high glucose exposure is termed glucotoxicity. The mechanisms of pancreatic beta-cell glucotoxicity involve in oxidative stress, endoplasmic reticulum stress, mitochrondrial dysfunction, inflammation, advanced glycation end products, hypoxia and activation of HIF-1a, and loss of differentiation in the alteration of beta-cell phenotype. The role of oxidative stress, endoplasmic reticulum stress, and loss of differentiation in the alteration of beta-cell phenotype is well ascertained. Oxidative stress is the central mechanism for glucotoxicity in pancreatic beta cells in diabetes.

关 键 词：胰岛Β细胞 葡萄糖毒性 分子机制 

分 类 号：R587.1[医药卫生—内分泌]