ER stress and the JNK pathway in insulin resistance
نویسندگان
چکیده
*Correspondence: Hideaki Kaneto, MD, PhD, Department of Internal Medicine and Therapeutics, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan; Tel. (81-6) 6879-3633; Fax (81-6) 6879-3639; e-mail: [email protected]
منابع مشابه
Endoplasmic reticulum stress links obesity, insulin action, and type 2 diabetes.
Obesity contributes to the development of type 2 diabetes, but the underlying mechanisms are poorly understood. Using cell culture and mouse models, we show that obesity causes endoplasmic reticulum (ER) stress. This stress in turn leads to suppression of insulin receptor signaling through hyperactivation of c-Jun N-terminal kinase (JNK) and subsequent serine phosphorylation of insulin receptor...
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The endoplasmic reticulum (ER) is an organelle that functions to synthesize, fold, and transport proteins. ER stress is a key link between type 2 diabetes (T2D), obesity, and insulin resistance. In this study, we investigated the effect of WHW on the ER stress response and the insulin signaling pathway in 3T3-L1 preadipocytes. 3T3-L1 preadipocytes were differentiated into adipocytes, and ER str...
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Hepatic insulin resistance has been attributed to both increased endoplasmic reticulum (ER) stress and accumulation of intracellular lipids, specifically diacylglycerol (DAG). The ER stress response protein, X-box-binding protein-1 (XBP1), was recently shown to regulate hepatic lipogenesis, suggesting that hepatic insulin resistance in models of ER stress may result from defective lipid storage...
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