AMPK activation regulates apoptosis, adipogenesis, and lipolysis by eIF2α in adipocytes
作者： Yossi Dagon , Yosefa Avraham , Elliot M. Berry
DOI: 10.1016/J.BBRC.2005.11.159
关键词:
摘要: AMP-activated protein kinase (AMPK) is a metabolic master switch regulating glucose and lipid metabolism. Recently, AMPK has been implicated in the control of adipose tissue content. Yet, nature this action controversial. We examined effect on F442a adipocytes activator-AICAR. Activation induced dose-dependent apoptotic cell death, inhibition lipolysis, downregulatation key adipogenic genes, such as peroxisome proliferator-activated receptor (PPARgamma) CCAAT/enhancer-binding alpha (C/EBPalpha). have identified alpha-subunit eukaryotic initiation factor-2 (eIF2alpha) target gene which phosphorylated following AICAR treatment. Such phosphorylation one best-characterized mechanisms for downregulating synthesis. 2-Aminopurine (2-AP), an inhibitor eIF2alpha kinases, could overcome AICAR, abolishing reduction PPARgamma C/EBPalpha lipolytic properties AMPK. Thus, may diminish adiposity via fat number through eIF2alpha-dependent translation shutdown.
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