title: AMPK: Lessons from transgenic and knockout animals.
abstract: 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.
authors.affiliation: Institut Cochin, Universite Paris Descartes, CNRS (UMR 8104), Department Endocrinology, Metabolism and Cancer, Paris, France. viollet@cochin.inserm.fr
authors.forename: Benoit
authors.initials: B
authors.lastname: Viollet
authors.forename: Yoni
authors.initials: Y
authors.lastname: Athea
authors.forename: Remi
authors.initials: R
authors.lastname: Mounier
authors.forename: Bruno
authors.initials: B
authors.lastname: Guigas
authors.forename: Elham
authors.initials: E
authors.lastname: Zarrinpashneh
authors.forename: Sandrine
authors.initials: S
authors.lastname: Horman
authors.forename: Louise
authors.initials: L
authors.lastname: Lantier
authors.forename: Sophie
authors.initials: S
authors.lastname: Hebrard
authors.forename: Jocelyne
authors.initials: J
authors.lastname: Devin-Leclerc
authors.forename: Christophe
authors.initials: C
authors.lastname: Beauloye
authors.forename: Marc
authors.initials: M
authors.lastname: Foretz
authors.forename: Fabrizio
authors.initials: F
authors.lastname: Andreelli
authors.forename: Renee
authors.initials: R
authors.lastname: Ventura-Clapier
authors.forename: Luc
authors.initials: L
authors.lastname: Bertrand
mesh_terms: D055372:AMP-Activated Protein Kinases / Q000737:chemistry / Q000378:metabolism*; D000273:Adipose Tissue / Q000201:enzymology; D000818:Animals; D030801:Animals, Genetically Modified; D001808:Blood Vessels / Q000201:enzymology / Q000502:physiology; D004734:Energy Metabolism; D055786:Gene Knockout Techniques; D006801:Humans; D007004:Hypoglycemic Agents / Q000494:pharmacology; D007031:Hypothalamus / Q000201:enzymology; D007333:Insulin Resistance; D008099:Liver / Q000201:enzymology; D023421:Models, Animal; D018482:Muscle, Skeletal / Q000201:enzymology; D009206:Myocardium / Q000201:enzymology; D011487:Protein Conformation
chemical_list: D007004:Hypoglycemic Agents; D055372:AMP-Activated Protein Kinases