Role of energy charge and AMP-activated protein kinase in adipocytes in the control of body fat stores

摘要: As indicated by in vitro studies, both lipogenesis and lipolysis adipocytes depend on the cellular ATP levels. Ectopic expression of mitochondrial uncoupling protein 1 (UCP1) white adipose tissue aP2-Ucp1 transgenic mice reduced obesity induced genetic or dietary manipulations. Furthermore, respiratory lowered energy charge adipocytes, while synthesis fatty acids (FA) was inhibited their oxidation increased. Importantly, complex metabolic changes triggered ectopic UCP1 were associated with activation AMP-activated kinase (AMPK), a master switch, adipocytes. Effects several typical treatments that reduce adiposity, such as administration leptin, beta-adrenoceptor agonists, bezafibrate, n-3 polyunsaturated FA fasting, can be compared phenotype mice. These situations generally lead to upregulation UCPs suppression On other hand, is Moreover, it has been shown AMPK activated adipocyte-derived hormones leptin adiponectin, also insulin-sensitizes thiazolidinediones. Thus, evident metabolism itself important for control body fat content are involved lipid The reciprocal link between represents prospective target new treatment strategies aimed at reducing obesity.