2. Academic Validation
  3. Oxidative stress, ER stress, and the JNK pathway in type 2 diabetes

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

  • J Mol Med (Berl). 2005 Jun;83(6):429-39. doi: 10.1007/s00109-005-0640-x.
Hideaki Kaneto 1,  Taka-Aki Matsuoka,  Yoshihisa Nakatani,  Dan Kawamori,  Takeshi Miyatsuka,  Munehide Matsuhisa,  Yoshimitsu Yamasaki
Affiliations

Affiliation

  • 1 Department of Internal Medicine and Therapeutics, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka, 565-0871, Japan. kaneto@medone.med.osaka-u.ac.jp
PMID: 15759102 DOI: 10.1007/s00109-005-0640-x
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.

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