Heat Shock Response Regulates Insulin Sensitivity and Glucose Homeostasis: Pathophysiological Impact and Therapeutic Potential
Heat Shock Response Regulates Insulin Sensitivity and Glucose Homeostasis: Pathophysiological Impact and Therapeutic Potential
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DOI：
10.2174/157339911796397811
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发表时间：
2011-01-01
影响因子：
3.3
通讯作者：
Araki, Eiichi
中科院分区：
文献类型：
--
作者：
Kondo, Tatsuya;Koga, Saori;Araki, Eiichi
全世界有越来越多的人患有肥胖、代谢综合征（MS）和2型糖尿病（T2 DM）。热休克反应（HSR）最初被认为是一种细胞防御机制，其减弱是代谢异常恶化的关键因素之一。另一方面，激活HSR增加热休克蛋白72（HSP 72）表达并改善啮齿动物和人类的胰岛素抵抗和葡萄糖稳态，这可能是通过抑制应激激酶如c-jun末端激酶（JNK）和κ B激酶β（IKK β）抑制剂的激活。这些方法还可以减少炎性细胞因子的产生，并防止动脉粥样硬化并发症的发生。本文综述了HSR在调节胰岛素敏感性和高血糖中的生理作用，以及HSR系统治疗MS和T2 DM以及其他细胞应激相关疾病的潜力。
A large and increasing number of people in all over the world suffer from obesity, metabolic syndrome (MS) and type 2 diabetes mellitus (T2DM). Attenuation of the heat shock response (HSR), which was originally identified as a cellular defense mechanism, is one of the key factors involved in the deterioration of metabolic abnormalities. On the other hand, activating the HSR increases heat shock protein 72 (HSP72) expression and improves insulin resistance and glucose homeostasis in rodents and humans, possibly by inhibiting the activation of stress kinases such as c-jun terminal kinase (JNK) and inhibitor of kappa B kinase beta(IKK beta). These approaches may also reduce inflammatory cytokine production and prevent the onset of atherogenic complications. This review focuses on the physiological effects of HSR in regulating insulin sensitivity and hyperglycemia, and the potential to target the HSR system for the treatment of MS and T2DM, as well as other cellular stress-related diseases.