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Received February 27, 2006
Revised March 17, 2006
Accepted after revision April 26, 2006
1 Institut Cochin, INSERM U567, CNRS UMR8104, Université René Descartes Paris 5, France
2 Institut Cochin, INSERM U567, CNRS UMR8104, Université René Descartes Paris 5, France
3 Hormone and Metabolic Research Unit, Institute of Cellular Pathology, Brussels
4 Division of Cardiology, School of Medicine, Université catholique de Louvain, Brussels
* To whom correspondence should be addressed. E-mail: viollet{at}cochin.inserm.fr.
It is now becoming evident that liver exerts an important role in the control of whole body energy nutrients metabolism. In this review, we focus on recent findings showing that AMP-activated protein kinase (AMPK) play 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 effect on phosphorylation of regulatory proteins and by long-term effect on gene expression. Activation of AMPK in the liver leads to the stimulatation of fatty acid oxidation and inhibition of lipogenesis, glucose production and protein synthesis. The medical interest in the AMPK system was recently increased after demonstration that AMPK could mediated some effects of the fat cell-derived adiponectin and the antidiabetic drugs, metformin and thiazolidinediones. These findings reinforces the idea that pharmacological activation of AMPK may provide, through signaling, metabolic and gene expression effects a new strategy for the management of metabolic hepatic disorders linked to type 2 diabetes and obesity.
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