title: The JNK pathway as a therapeutic target for diabetes.
abstract: The hallmark of Type 2 diabetes is insulin resistance and pancreatic beta-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 beta-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 beta-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 beta-cell dysfunction and, thus, could be a potential therapeutic target for diabetes.
authors.affiliation: Department of Internal Medicine and Therapeutics (A8), Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan. kaneto@medone.med.osaka-u.ac.jp
authors.forename: Hideaki
authors.initials: H
authors.lastname: Kaneto
mesh_terms: D003924:Diabetes Mellitus, Type 2 / Q000188:drug therapy*; D006801:Humans; D007004:Hypoglycemic Agents / Q000494:pharmacology*; D007328:Insulin / Q000378:metabolism; D048670:MAP Kinase Kinase 4 / Q000037:antagonists & inhibitors* / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects*
chemical_list: D007004:Hypoglycemic Agents; D007328:Insulin; D048670:MAP Kinase Kinase 4