Cited by 315Metabolism, Diabetes, and CancerPeroxisome Proliferator-Activated ReceptorsAdipose Tissue and Metabolism

AMPK: Lessons from transgenic and knockout animals

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Viollet, Benoit·2009·Frontiers in bioscience

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.

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  • Double knockout of AMPKα1 and AMPKα2 in mice gives rise to embryonic lethality.

    “The α-subunit is essential, and a double knockout (KO) of AMPKα1 and AMPKα2 in mice gives rise to embryonic lethality [24].”

    From AMPK, Mitochondrial Function, and Cardiovascular Disease (2020) · cites this paper as [24]

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  1. M. Foretz, N. Taleux, B. Guigas, S. Horman, C. Beauloye, F. Andreelli, L. Bertrand, B. Viollet: Regulation of energy metabolism by AMPK: a novel therapeutic approach for the treatment of metabolic and cardiovascular diseases. Med Sci 22(4):381-8 (2006)

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Authors
Viollet, B.
Venue
Frontiers in bioscience
Publisher
IMR Press
Published
2009
Volume
Volume
Issue
14
Pages
19
ISSN
  • 1093-4715 (ISSN-L)
  • 1093-9946
OpenAlex
W2104083311
Cited by
314
References
157
Citations by year
2026: 6 · 2025: 11 · 2024: 14 · 2023: 7 · 2022: 21 · 2021: 18 · 2020: 20 · 2019: 9 · 2018: 21 · 2017: 15 · 2016: 20 · 2015: 27 · 2014: 22 · 2013: 32 · 2012: 20
FWCI
1.79
Type
journal article
Language
en
Open access
Licence
cc-by
Locations
  • Frontiers in bioscience (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
  • HAL (submittedVersion, cc-by)
  • DIAL (Catholic University of Leuven) (submittedVersion, other-oa)
Funders
  • European Commission (LSHMCT-2004-005272)
  • Agence Nationale de la Recherche
  • Institut National de la Santé et de la Recherche Médicale
  • Fondation de France
  • Fonds Spéciaux de Recherche
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
  • Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
Keywords
AMPK, energy metabolism, energy homeostasis, AMPK knockout mice, AMPK signaling, fatty acid oxidation, glycolysis, lipogenesis, ATP depletion, gene expression regulation
MeSH terms
Adipose Tissue, Animals, Blood Vessels, Energy Metabolism, Humans, Hypoglycemic Agents, Hypothalamus, Insulin Resistance, Liver, Myocardium, Protein Conformation, Muscle, Skeletal, Models, Animal, Animals, Genetically Modified, AMP-Activated Protein Kinases, Gene Knockout Techniques

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