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Cited by 242Metabolism, Diabetes, and CancerPancreatic function and diabetesAdipose Tissue and Metabolism

The DOI matches its Crossref record.

Physiological role of AMP-activated protein kinase (AMPK): insights from knockout mouse models

Viollet, B., Andreelli, F., Jørgensen, S.B., Perrin, C., Flamez, D., Mu, J., Wojtaszewski, J.F.P., Schuit, F.C., Birnbaum, M., Richter, E., Burcelin, R., Vaulont, S.·2003·Biochemical Society Transactions
DOI 10.1042/bst0310216
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Abstract

AMP-activated protein kinase (AMPK) is viewed as a fuel sensor for glucose and lipid metabolism. To understand better the physiological role of the catalytic AMPK subunit isoforms, we generated two knockout mouse models with the α1 (AMPKα1−/−) and α2 (AMPKα2−/−) catalytic subunit genes deleted. No defect in glucose homoeostasis was observed in AMPKα1−/− mice. On the other hand, AMPKα2−/− mice presented high plasma glucose levels and low plasma insulin concentrations in the fed period and during the glucose tolerance test. Nevertheless, in isolated AMPKα2−/− pancreatic islets, glucose-stimulated insulin secretion was not affected. Surprisingly, AMPKα2−/− mice were insulin-resistant and had reduced muscle glycogen synthesis as assessed in vivo by the hyperinsulinaemic euglycaemic clamp procedure. Reduction of insulin sensitivity and glycogen synthesis were not dependent on the lack of AMPK in skeletal muscle, since mice expressing a dominant inhibitory mutant of AMPK in skeletal muscle were not affected and since insulin-stimulated glucose transport in incubated muscles in vitro was normal in AMPKα2−/− muscles. Furthermore, AMPKα2−/− mice have a higher sympathetic tone, as shown by increased catecholamine urinary excretion. Increased adrenergic tone could explain both decreased insulin secretion and insulin resistance observed in vivo in AMPKα2−/− mice. We suggest that the α2 catalytic subunit of AMPK plays a major role as a fuel sensor by modulating the activity of the autonomous nervous system in vivo.

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Authors
Viollet, B., Andreelli, F., Jørgensen, S. B., Perrin, C., Flamez, D., Mu, J., Wojtaszewski, J. F. P., Schuit, F. C., Birnbaum, M., Richter, E., Burcelin, R., & Vaulont, S.
Affiliations
  • Institut Cochin (FR)
  • Institut Cochin, Dpt GDPM, 24 rue du faubourg Saint-Jacques 75014 Paris, France
  • University of Copenhagen (DK)
  • Centre National de la Recherche Scientifique (FR)
  • Diabetes Research Center, Brussels, Belgium
  • Howard Hughes Medical Institute (US)
Corresponding author
  • Viollet, B.
  • Vaulont, S.
ORCID
Venue
Biochemical Society Transactions
Publisher
Portland Press Ltd.
Published
2003-02-01
Volume
31
Issue
1
Pages
216-219
ISSN
  • 0300-5127 (ISSN-L)
  • 1470-8752
DOI
10.1042/bst0310216
OpenAlex
W2060836453
Cited by
241
References
0
Citations by year
2026: 2 · 2024: 3 · 2023: 2 · 2022: 8 · 2021: 13 · 2020: 8 · 2019: 8 · 2018: 11 · 2017: 10 · 2016: 12 · 2015: 8 · 2014: 19 · 2013: 19 · 2012: 21
FWCI
2.77
Type
journal article
Language
en
Open access
closed
Locations
  • Biochemical Society Transactions (publishedVersion)
  • PubMed (publishedVersion)
  • Ghent University Academic Bibliography (Ghent University) (submittedVersion)
  • Research at the University of Copenhagen (University of Copenhagen) (submittedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pancreatic function and diabetes
  • Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
Keywords
AMPK, glucose homeostasis, insulin resistance, glucose-stimulated insulin secretion, pancreatic islets, muscle glycogen synthesis, insulin sensitivity, sympathetic nervous system, catecholamine excretion, knockout mice
MeSH terms
Animals, Glucose Tolerance Test, Glycogen, Mice, Transgenic, Models, Biological, Multienzyme Complexes, Mutation, Protein Serine-Threonine Kinases, Mice, Knockout, Muscle, Skeletal, Catalytic Domain, Mice, AMP-Activated Protein Kinases

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