氧化应激与2型糖尿病的研究进展

被引：24

作者：

李爱琴

陆环

徐文静

谢建新

机构：

[1] 石河子大学医学院新疆地方病与民族高发病省部共建重点实验室

来源：

现代生物医学进展 | 2010年 / 10卷 / 12期

关键词：

氧化应激; 活性氧族; 胰岛素抵抗; 2型糖尿病;

D O I：

10.13241/j.cnki.pmb.2010.12.033

中图分类号：

R587.1 [糖尿病];

学科分类号：

摘要：

氧化应激与2型糖尿病(T2DM)的发生、发展密切相关。胰岛素抵抗(Insulin Resistance,IR)、胰岛β细胞功能受损是2型糖尿病的主要病因。而氧化应激可以直接及间接激活细胞内的一系列应激信号通路,如核因子κ-B(Nuclear factor-KappaB,NF-κB)、c-Jun氨基端激酶(NH-terminal Jun kinase,JNK)、蛋白激酶C(protein kinaseC,PKC)、p38丝裂原活化蛋白激酶(Mitogen-activated protein kinase,MAPK)等。这些应激通路的激活可以产生以下结果:(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,致胰岛素合成和分泌减少;(3)促进胰岛β细胞凋亡等。本文针对氧化应激诱导胰岛素抵抗和胰岛β细胞功能受损等机制加以综述,以便进一步阐明2型糖尿病的发病机制。

引用

页码：2371 / 2372+2378 +2378

页数：3

共 14 条

[1]

Chronic exposure to free fatty acid or high glucose induces apoptosis in rat pancreatic islets: possible role of oxidative stress. Piro S, Anello M, Di Pietro C, et al. Metabolism . 2002

[2]

Role of mitochondria in toxic oxidative stress. Fariss MW, Chan CB, Patel M, et al. Molecular Interventions . 2005

[3]

Chronic exposure to free fatty acids or high glucose induces apoptosis in rat pancreatic islets: Possible role of oxidative stress[J] . Salvatore Piro,Marcello Anello,Cinzia Di Pietro,Maria Natalia Lizzio,Giovanni Patan[egrave],Agata Maria Rabuazzo,Riccardo Vigneri,Michele Purrello,Francesco Purrello. &nbspMetabolism . 2002 (10)

[4]

Diabetes[P]. 英国专利:GB201117172D0,2011-11-16

[5]

Reactive species and early manifestation of insulin resistance in type2diabetes. Fridiyand LE,Philipson LH. Diabetes,Obesity and Metabolism . 2006

[6]

A significant portion of mitochondrial proton leak in intact thymocytes depends on expression of UCP2. Krauss S, Zhang CY, Lowell BB. Proceedings of the National Academy of Sciences of the United States of America . 2002

[7]

Free fatty acids trigger apoptosis and inhibit cell cycle progression in human vascular endothelial cells. Artwohl M, Roden M, Waldhausl W, et al. The FASEB Journal . 2004

[8]

Mitochondrial dysfunction and type 2 diabetes. Lowell BB, Shulman GI. Science . 2005

[9]

Reactive oxygen species have a causal role in multiple forms of insulin resistance. Houstis N, Rosen ED, Lander ES. Nature . 2006

[10]

Association of oxidative stress,insulin resistance and diabetes risk phenotypes:the Framingham offspring study. Meigs JB,Larson MG,Fox CS, et a. Diabetes Care . 2007

← 1 2 →