| Literature DB >> 15759102 |
Hideaki Kaneto1, Taka-Aki Matsuoka, Yoshihisa Nakatani, Dan Kawamori, Takeshi Miyatsuka, Munehide Matsuhisa, Yoshimitsu Yamasaki.
Abstract
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.Entities:
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Year: 2005 PMID: 15759102 DOI: 10.1007/s00109-005-0640-x
Source DB: PubMed Journal: J Mol Med (Berl) ISSN: 0946-2716 Impact factor: 4.599