Oxidative stress, ER stress, and the JNK pathway in type 2 diabetes

被引：162

作者：

Kaneto, H ^{[1
]}

Matsuoka, T ^{[1
]}

Nakatani, Y ^{[1
]}

Kawamori, D ^{[1
]}

Miyatsuka, T ^{[1
]}

Matsuhisa, M ^{[1
]}

Yamasaki, Y ^{[1
]}

机构：

[1] Osaka Univ, Dept Internal Med & Therapeut, Grad Sch Med, Suita, Osaka 5650871, Japan

来源：

JOURNAL OF MOLECULAR MEDICINE-JMM | 2005年 / 83卷 / 06期

关键词：

oxidative stress; ER stress; JNK pathway; insulin biosynthesis; insulin resistance;

D O I：

10.1007/s00109-005-0640-x

中图分类号：

Q3 [遗传学];

学科分类号：

071007 ; 090102 ;

摘要：

Pancreatic beta-cell dysfunction and insulin resistance are observed in type 2 diabetes. Under diabetic conditions, oxidative stress and ER stress are induced in various tissues, leading to activation of the JNK pathway. This JNK activation suppresses insulin biosynthesis and interferes with insulin action. Indeed, suppression of the JNK pathway in diabetic mice improves insulin resistance and ameliorates glucose tolerance. Thus, the JNK pathway plays a central role in pathogenesis of type 2 diabetes and may be a potential target for diabetes therapy.

引用

页码：429 / 439

页数：11

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