Author: Kaneto, Hideaki

Source: Expert Opinion on Therapeutic Targets, Volume 9, Number 3, 1 June 2005 , pp. 581-592(12)

Publisher: Informa Healthcare

Abstract:

The hallmark of Type 2 diabetes is insulin resistance and pancreatic -cell dysfunction. Under diabetic conditions, the c-jun N-terminal kinase (JNK) pathway is activated in various tissues, which is involved in both insulin resistance and -cell dysfunction. Activation of the JNK pathway interferes with insulin action and reduces insulin biosynthesis, and suppression of the JNK pathway in diabetic mice improves insulin resistance and -cell function, leading to amelioration of glucose tolerance. Taken together, the JNK pathway is likely to play a central role in the progression of insulin resistance and -cell dysfunc-tion and, thus, could be a potential therapeutic target for diabe-tes.

Keywords: diabetes; endoplasmic reticulum (ER) stress; insulin biosynthesis; insulin resistance; c-jun N-terminal kinase (JNK) pathway; oxidative stress

Document Type: Review article

DOI: http://dx.doi.org/10.1517/14728222.9.3.581

Publication date: 2005-06-01

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