کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2196231 1098802 2013 10 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
The role of AMP-activated protein kinase in regulating white adipose tissue metabolism
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی بیولوژی سلول
پیش نمایش صفحه اول مقاله
The role of AMP-activated protein kinase in regulating white adipose tissue metabolism
چکیده انگلیسی

AMP-activated protein kinase (AMPK) is a heterotrimeric enzyme that plays a major role in the maintenance of energy homeostasis in various organs and tissues. When activated, AMPK can induce substrate catabolism and shut down energy-consuming anabolic pathways to increase intracellular ATP availability. Even though most of these effects have been described in muscle and liver, several studies have provided compelling evidence that AMPK also plays an important role in the regulation of white adipose tissue (WAT) glucose and lipid metabolism. In fact, the effects of acute and chronic AMPK activation in the WAT induce profound changes in adiposity with important implications for the treatment of obesity and its related metabolic disorders. This review discusses the role of AMPK in the regulation of white adipocyte metabolism with respect to energy storage and release, gene expression, mitochondrial biogenesis, oxidative capacity, cell differentiation, and the potential impact on whole-body adiposity and energy homeostasis.


► Chronic AMPK activation increases mitochondrial density and oxidative capacity in white adipocytes.
► AMPK exerts an anti-lipogenic effect by regulating glucose and fatty acid uptake and metabolism in adipocytes.
► AMPK modulates adipocyte lipolysis by reducing and increasing HSL and ATGL activities, respectively.
► AMPK inhibits the proliferation and differentiation of white adipocytes.
► Chronic AICAR-induced AMPK activation reduces adiposity and potentiates the anorexic effect of leptin in vivo.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Molecular and Cellular Endocrinology - Volume 366, Issue 2, 25 February 2013, Pages 194–203
نویسندگان
,