کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
1940671 1050786 2006 5 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
AMPK activation regulates apoptosis, adipogenesis, and lipolysis by eIF2α in adipocytes
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی زیست شیمی
پیش نمایش صفحه اول مقاله
AMPK activation regulates apoptosis, adipogenesis, and lipolysis by eIF2α in adipocytes
چکیده انگلیسی

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, the nature of this action is controversial. We examined the effect on F442a adipocytes of the AMPK activator-AICAR. Activation of AMPK induced dose-dependent apoptotic cell death, inhibition of lipolysis, and downregulatation key adipogenic genes, such as peroxisome proliferator-activated receptor (PPARγ) and CCAAT/enhancer-binding protein alpha (C/EBPα). We have identified the α-subunit of the eukaryotic initiation factor-2 (eIF2α) as a target gene which is phosphorylated following AICAR treatment. Such phosphorylation is one of the best-characterized mechanisms for downregulating protein synthesis. 2-Aminopurine (2-AP), an inhibitor of eIF2α kinases, could overcome the apoptotic effect of AICAR, abolishing the reduction of PPARγ and C/EBPα and the lipolytic properties of AMPK. Thus, AMPK may diminish adiposity via reduction of fat cell number through eIF2α-dependent translation shutdown.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 340, Issue 1, 3 February 2006, Pages 43–47
نویسندگان
, , ,