Knockout of the α2 but Not α1 5′-AMP-activated Protein Kinase Isoform Abolishes 5-Aminoimidazole-4-carboxamide-1-β-4-ribofuranosidebut Not Contraction-induced Glucose Uptake in Skeletal Muscle
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We investigated the importance of the two catalytic alpha-isoforms of the 5'-AMP-activated protein kinase (AMPK) in 5-aminoimidazole-4-carboxamide-1-beta-4-ribofuranoside (AICAR) and contraction-induced glucose uptake in skeletal muscle. Incubated soleus and EDL muscle from whole-body alpha2- or alpha1-AMPK knockout (KO) and wild type (WT) mice were incubated with 2.0 mm AICAR or electrically stimulated to contraction. Both AICAR and contraction increased 2DG uptake in WT muscles. KO of alpha2, but not alpha1, abolished AICAR-induced glucose uptake, whereas neither KO affected contraction-induced glucose uptake. AICAR and contraction increased alpha2- and alpha1-AMPK activity in wild type (WT) muscles. During AICAR stimulation, the remaining AMPK activity in KO muscles increased to the same level as in WT. During contraction, the remaining AMPK activity in alpha2-KO muscles was elevated by 100% probably explained by a 2-3-fold increase in alpha1-protein. In alpha1-KO muscles, alpha2-AMPK activity increased to similar levels as in WT. Both interventions increased total AMPK activity, as expressed by AMPK-P and ACCbeta-P, in WT muscles. During AICAR stimulation, this was dramatically reduced in alpha2-KO but not in alpha1-KO, whereas during contraction, both measurements were essentially similar to WT in both KO-muscles. The results show that alpha2-AMPK is the main donor of basal and AICAR-stimulated AMPK activity and is responsible for AICAR-induced glucose uptake. In contrast, during contraction, the two alpha-isoforms seem to substitute for each other in terms of activity, which may explain the normal glucose uptake despite the lack of either alpha2- or alpha1-AMPK. Alternatively, neither alpha-isoform of AMPK is involved in contraction-induced muscle glucose uptake.
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AMPK α2, β2 and γ3 null and α2KD and β1β2 M-KO mice have normal insulin-stimulated glucose uptake in muscle.
“In support of this, insulin also does not increase AMPK T172 or ACC S79/212 phosphorylation [74] and AMPK α2, β2 and γ3 null and α2KD and β1β2 M-KO mice have normal insulin-stimulated glucose uptake in muscle [26,28,30,36,100] despite blunted TBC1D1 PAS and T590 phosphorylation in response to insulin [30,74].”
From AMPK and Exercise: Glucose Uptake and Insulin Sensitivity (2013) · cites this paper as [26]
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 [26]
Under basal conditions the α2 subunit rather than α1 subunit is required for AICAR-induced glucose uptake.
“The α2 subunit of AMPK is required for AICAR-induced inhibitory effects of mTOR signaling in skeletal muscle [159], which is consistent with alternative findings that showing that under basal conditions the α2 subunit rather than α1 subunit is required for AICAR-induced glucose uptake [26].”
From AMPK and Exercise: Glucose Uptake and Insulin Sensitivity (2013) · cites this paper as [26]
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Exercise-induced AMPK activity in skeletal muscle: Role in glucose uptake and insulin sensitivity
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Important role for AMPKαl in limiting skeletal muscle cell hypertrophy
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Self-citationHyaluronan Accumulates With High-Fat Feeding and Contributes to Insulin Resistance
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Activation of AMP kinase α1 subunit induces aortic vasorelaxation in mice
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Self-citationPrior exercise increases phosphorylation of Akt substrate of 160 kDa (AS160) in rat skeletal muscle
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Contraction regulates site-specific phosphorylation of TBC1D1 in skeletal muscle
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Brain-specific repression of AMPKα1 alleviates pathophysiology in Alzheimer’s model mice
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AMPK and TBC1D1 Regulate Muscle Glucose Uptake After, but Not During, Exercise and Contraction
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Self-citationAMP-Activated Protein Kinase Is Not Down-Regulated in Human Skeletal Muscle of Obese Females
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Self-citationThe role of ampk in controlling metabolism and mitochondrial biogenesis during exercise
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Self-citationLKB1 and AMPK and the regulation of skeletal muscle metabolism
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SIRT1 takes a backseat to AMPK in the regulation of insulin sensitivity by resveratrol
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Chronic elevated calcium blocks AMPK-induced GLUT-4 expression in skeletal muscle
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Self-citationAMPK activation regulates neuronal structure in developing hippocampal neurons
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Relaxin Treatment Reverses Insulin Resistance in Mice Fed a High-Fat Diet
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Potentiation of insulin-stimulated glucose transport by the AMP-activated protein kinase
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α1AMP-activated protein kinase mediates vascular protective effects of exercise
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Self-citationSkeletal muscle signaling response to sprint exercise in men and women
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- Authors
- Jørgensen, S. B., Viollet, B., Andreelli, F., Frøsig, C., Birk, J. B., Schjerling, P., Vaulont, S., Richter, E. A., & Wojtaszewski, J. F. P.
- Affiliations
- University of Copenhagen (DK)
- Rigshospitalet (DK)
- Centre National de la Recherche Scientifique (FR)
- Corresponding author
- Jørgensen, Sebastian B.
- ORCID
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2004-01
- Volume
- 279
- Issue
- 2
- Pages
- 1070-1079
- ISSN
- 0021-9258 (ISSN-L)
- OpenAlex
- W2073361547
- Cited by
- 553
- References
- 44
- Citations by year
- 2026: 7 · 2025: 8 · 2024: 5 · 2023: 7 · 2022: 10 · 2021: 16 · 2020: 24 · 2019: 11 · 2018: 16 · 2017: 23 · 2016: 30 · 2015: 33 · 2014: 23 · 2013: 30 · 2012: 38
- FWCI
- 13.87
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Biological Chemistry (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- 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 › Physiology › Adipose Tissue and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Keywords
- AMPK, AICAR, skeletal muscle glucose uptake, muscle contraction, AMPK knockout mice, soleus muscle, EDL muscle
- MeSH terms
- Aminoimidazole Carboxamide, Animals, Deoxyglucose, Dose-Response Relationship, Drug, Female, Glucose, Glucose Tolerance Test, Glycogen, Insulin, Male, Models, Genetic, Multienzyme Complexes, Muscles, Precipitin Tests, Ribonucleotides, Time Factors, Immunoblotting, Protein Serine-Threonine Kinases, Mice, Knockout, Muscle, Skeletal, Protein Isoforms, Mice, AMP-Activated Protein Kinases
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