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Activation of AMP‐activated protein kinase in the liver: a new strategy for the management of metabolic hepatic disorders
Author(s) -
Viollet Benoit,
Foretz Marc,
Guigas Bruno,
Horman Sandrine,
Dentin Renaud,
Bertrand Luc,
Hue Louis,
Andreelli Fabrizio
Publication year - 2006
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2006.108506
Subject(s) - ampk , lipogenesis , amp activated protein kinase , protein kinase a , beta oxidation , metformin , endocrinology , fatty liver , adiponectin , biology , lipid metabolism , kinase , chemistry , medicine , metabolism , microbiology and biotechnology , insulin , insulin resistance , disease
It is now becoming evident that the liver has an important role in the control of whole body metabolism of energy nutrients. In this review, we focus on recent findings showing that AMP‐activated protein kinase (AMPK) plays a major role in the control of hepatic metabolism. AMPK integrates nutritional and hormonal signals to promote energy balance by switching on catabolic pathways and switching off ATP‐consuming pathways, both by short‐term effects on phosphorylation of regulatory proteins and by long‐term effects on gene expression. Activation of AMPK in the liver leads to the stimulation of fatty acid oxidation and inhibition of lipogenesis, glucose production and protein synthesis. Medical interest in the AMPK system has recently increased with the demonstration that AMPK could mediate some of the effects of the fat cell‐derived adiponectin and the antidiabetic drugs metformin and thiazolidinediones. These findings reinforce the idea that pharmacological activation of AMPK may provide, through signalling and metabolic and gene expression effects, a new strategy for the management of metabolic hepatic disorders linked to type 2 diabetes and obesity.