自噬、氧化应激与2型糖尿病的关系  

Associations of Type 2 Diabetes Mellitus with Autophagy and Oxidative Stress

作　　者：于顺 倪月秋[2] 

机构地区：[1]沈阳医学院基础医学院,辽宁沈阳110034 [2]沈阳医学院基础医学院生理学教研室,辽宁沈阳110034

出　　处：《沈阳医学院学报》2018年第1期93-96,共4页Journal of Shenyang Medical College

基　　金：国家自然科学基金(No.81273809);沈阳医学院大学生科研项目(No.20179016)

摘　　要：自噬是一种依赖溶酶体途径的代谢过程,能够降解、清除细胞内的长效蛋白及受损细胞器,维持细胞内稳态。氧化应激是指机体的氧化平衡状态紊乱,机体倾向于氧化状态,从而造成组织细胞损伤。目前,2型糖尿病主要发病原因被认为是胰岛素分泌功能障碍和胰岛素抵抗合并存在。有研究表明,氧化应激和自噬在胰岛β细胞功能受损和胰岛素抵抗中发挥重要作用。氧化应激与自噬也有着密切的联系,氧化应激可诱导自噬,而自噬可通过吞噬和降解产生的氧化物来降低氧化应激损伤,在维持胰岛β细胞结构和功能,以及降低胰岛素抵抗中发挥了重要作用。Autophagy is a lysosomal degradation pathway that can degrade and recycle long-lived proteins and damaged organelles to maintain intracellular homeostasis. Oxidative stress is a state of unbalanced tissue oxidation leading to an imbalance between antioxidants and oxidants. Disturbances in the normal redox state of cells can cause toxic effects that damage all components of the cell, including proteins, lipids,and DNA. Type 2 diabetes mellitus(T2 DM) is a heterogenous disorder caused by a combination of insulin resistance and impaired insulin secretion. Oxidative stress and autophagy have been suggested as mechanisms for pancreatic β-cells injury and insulin resistance in T2 DM. Oxidative stress can also promote the formation of autophagy.Autophagy, in turn, may contribute to reduce oxidative damages by degradating oxidized substance,which is necessary to improve the function of pancreatic β-cells and reduce insulin resistance.

关 键 词：自噬 氧化应激 2型糖尿病 胰岛素抵抗 胰岛Β细胞 

分 类 号：R587.1[医药卫生—内分泌]