HSP AND DIABETES
作者： Martin Whitham , Mark A. Febbraio
DOI: 10.1007/978-90-481-3381-9_1
关键词: Insulin receptor substrate 、 Endocrinology 、 ASK1 、 Kinase 、 Protein kinase C 、 Insulin resistance 、 Insulin receptor 、 IκB kinase 、 Biology 、 IRS2 、 Internal medicine
摘要: As the prevalence of diabetes continues to rise, strategies that aim prevent and treat condition continue gain importance. Obesity is thought induce a state low-grade inflammation, which ultimately disrupts insulin signalling predisposes individuals type II diabetes. In particular, TNFα, endoplasmic reticulum (ER) oxidative stress all appear be associated with obesity stimulate inflammatory kinases such as c jun amino terminal kinase (JNK), inhibitor NF-κβ (IKK) protein C (PKC). These in turn inhibit signalling, predominantly through inhibitory phosphorylation receptor substrate (IRS). The current chapter reviews literature describes this process potential heat shock proteins have preventing disruption signalling. data are presented demonstrate role Hsp72 prevention resistance diet genetic models murine obesity. HSP autoimmunity I also discussed
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