IMR Press / FBL / Volume 14 / Issue 1 / DOI: 10.2741/3229

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Article
AMPK: Lessons from transgenic and knockout animals
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1 Institut Cochin, Universite Paris Descartes, CNRS (UMR 8104), Department Endocrinology, Metabolism and Cancer, Paris, France
2 Inserm, U567, Paris, France
3 Inserm, U769, Chatenay-Malabry, France
4 Universite Paris-Sud, Chatenay-Malabry, France
5 Universite catholique de Louvain and Institute of Cellular Pathology, Hormone and Metabolic Research Unit, Brussels, Belgium
6 Leiden University Medical Center, Department of Mol Cell Biology, Leiden, Netherland
7 Universite catholique de Louvain, Division of cardiology, Brussels, Belgium
8 Inserm U695, IFR Xavier Bichat, Paris, France
Academic Editors:Bruce Kemp, Stuart Macaulay
Front. Biosci. (Landmark Ed) 2009, 14(1), 19–44;
Published: 1 January 2009
(This article belongs to the Special Issue AMP-activated protein kinase)

AMP-activated protein kinase (AMPK), a phylogenetically conserved serine/threonine protein kinase, has been proposed to function as a fuel gauge to monitor cellular energy status in response to nutritional environmental variations. AMPK system is a regulator of energy balance that, once activated by low energy status, switches on ATP-producing catabolic pathways (such as fatty acid oxidation and glycolysis), and switches off ATP-consuming anabolic pathways (such as lipogenesis), both by short-term effect on phosphorylation of regulatory proteins and by long-term effect on gene expression. Numerous observations obtained with pharmacological activators and agents that deplete intracellular ATP have been supportive of AMPK playing a role in the control of energy metabolism but none of these studies have provided conclusive evidence. Relatively recent developments in our understanding of precisely how AMPK complexes might operate to control energy metabolism is due in part to the development of transgenic and knockout mouse models. Although there are inevitable caveats with genetic models, some important findings have emerged. In the present review, we discuss recent findings obtained from animal models with inhibition or activation of AMPK signaling pathway.

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