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Cited by 57Metabolism, Diabetes, and CancerAdipose Tissue and MetabolismMuscle Physiology and Disorders

The α-subunit of AMPK is essential for submaximal contraction-mediated glucose transport in skeletal muscle in vitro

Lefort, Natalie, St.-Amand, Emmanuelle, Morasse, Sébastien, Côté, Claude H., Marette, André·2008·American Journal of Physiology-Endocrinology and Metabolism
DOI 10.1152/ajpendo.90362.2008
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Abstract

AMP-activated protein kinase (AMPK) is a key signaling protein in the regulation of skeletal muscle glucose uptake, but its role in mediating contraction-induced glucose transport is still debated. The effect of contraction on glucose transport is impaired in EDL muscle of transgenic mice expressing a kinase-dead, dominant negative form of the AMPKα 2 subunit (KD-AMPKα 2 mice). However, maximal force production is reduced in this muscle, raising the possibility that the defect in glucose transport was due to a secondary decrease in force production and not impaired AMPKα 2 activity. Generation of force-frequency curves revealed that muscle force production is matched between wild-type (WT) and KD-AMPKα 2 mice at frequencies ≤50 Hz. Moreover, AMPK activation is already maximal at 50 Hz in muscles of WT mice. When EDL muscles from WT mice were stimulated at a frequency of 50 Hz for 2 min (200-ms train, 1/s, 30 volts), contraction caused an ∼3.5-fold activation of AMPKα 2 activity and an ∼2-fold stimulation of glucose uptake. Conversely, whereas force production was similar in EDL of KD-AMPKα 2 animals, no effect of contraction was observed on AMPKα 2 activity, and glucose uptake stimulation was reduced by 50% ( P < 0.01) As expected, 5-aminoimidazole-4-carboxamide-1-β-d-ribofuranosyl 5′-monophosphate (AICAR) caused a 2.3-fold stimulation of AMPKα 2 activity and a 1.7-fold increase in glucose uptake in EDL from WT mice, whereas no effect was detected in muscle from KD-AMPKα 2 mice. These data demonstrate that AMPK activation is essential for both AICAR and submaximal contraction-induced glucose transport in skeletal muscle but that AMPK-independent mechanisms are also involved.

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Crossref · 10.1152/ajpendo.90362.2008

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  • AMPK α2 KO and α2 KD and α2iTg mice have normal or only modest reductions in glucose uptake during contractions.

    “AMPK α2 KO and α2 KD and α2iTg mice have normal or only modest reductions in glucose uptake during contractions [4,26,31,32,118-120].”

    From AMPK and Exercise: Glucose Uptake and Insulin Sensitivity (2013) · cites this paper as [119]

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Authors
Lefort, N., St.-Amand, E., Morasse, S., Côté, C. H., & Marette, A.
Affiliations
Université Laval (CA)
ORCID
Venue
American Journal of Physiology-Endocrinology and Metabolism
Publisher
American Physiological Society
Published
2008-12
Volume
295
Issue
6
Pages
E1447-E1454
ISSN
  • 0193-1849 (ISSN-L)
  • 1522-1555
DOI
10.1152/ajpendo.90362.2008
OpenAlex
W2162834706
Cited by
57
References
44
Citations by year
2026: 2 · 2022: 1 · 2021: 2 · 2020: 2 · 2019: 2 · 2018: 2 · 2017: 3 · 2016: 4 · 2015: 4 · 2014: 6 · 2013: 6 · 2012: 5
FWCI
2.46
Type
journal article
Language
en
Open access
closed
Locations
  • American Journal of Physiology-Endocrinology and Metabolism (publishedVersion)
  • PubMed (publishedVersion)
Funders
Canadian Diabetes Association
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
  • Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
Keywords
AMPK, skeletal muscle glucose uptake, EDL muscle, AICAR, muscle force production, force-frequency relationship
MeSH terms
Aminoimidazole Carboxamide, Animals, Biological Transport, Glucose, Muscle Contraction, Physical Stimulation, Ribonucleotides, Mice, Knockout, Muscle, Skeletal, Mice, AMP-Activated Protein Kinases

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