The AMP-activated protein kinase α2 catalytic subunit controls whole-body insulin sensitivity
Open accessAbstract
AMP-activated protein kinase (AMPK) is viewed as a fuel sensor for glucose and lipid metabolism. To better understand the physiological role of AMPK, we generated a knockout mouse model in which the AMPKalpha2 catalytic subunit gene was inactivated. AMPKalpha2(-/-) mice presented high glucose levels in the fed period and during an oral glucose challenge associated with low insulin plasma levels. However, in isolated AMPKalpha2(-/-) pancreatic islets, glucose- and L-arginine-stimulated insulin secretion were not affected. AMPKalpha2(-/-) mice have reduced insulin-stimulated whole-body glucose utilization and muscle glycogen synthesis rates assessed in vivo by the hyperinsulinemic euglycemic clamp technique. Surprisingly, both parameters were not altered in mice expressing a dominant-negative mutant of AMPK in skeletal muscle. Furthermore, glucose transport was normal in incubated isolated AMPKalpha2(-/-) muscles. These data indicate that AMPKalpha2 in tissues other than skeletal muscles regulates insulin action. Concordantly, we found an increased daily urinary catecholamine excretion in AMPKalpha2(-/-) mice, suggesting altered function of the autonomic nervous system that could explain both the impaired insulin secretion and insulin sensitivity observed in vivo. Therefore, extramuscular AMPKalpha2 catalytic subunit is important for whole-body insulin action in vivo, probably through modulation of sympathetic nervous activity.
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AMPK α2 KO and α2KD mice have reduced AMPK T172 phosphorylation and α2 activity in skeletal muscle.
“AMPK α2 KO and α2KD mice have reduced AMPK T172 phosphorylation and α2 activity in skeletal muscle, but enhanced or modestly reduced α1 activity, respectively [31,33,34].”
From AMPK and Exercise: Glucose Uptake and Insulin Sensitivity (2013) · cites this paper as [33]
AMPK α1 KO and α2KD mice have normal insulin sensitivity on a chow and high-fat diet.
“AMPK α1 KO and α2KD mice have normal insulin sensitivity on a chow and high-fat diet [33,36].”
From AMPK and Exercise: Glucose Uptake and Insulin Sensitivity (2013) · cites this paper as [33]
Whole-body AMPK α2 KO mice have reduced insulin secretion and whole-body insulin-stimulated glucose utilization due to elevated catecholamine levels and a hyperactive sympathetic nervous system.
“Whole-body AMPK α2 KO mice have reduced insulin secretion and whole-body insulin-stimulated glucose utilization due to elevated catecholamine levels and a hyperactive sympathetic nervous system [33].”
From AMPK and Exercise: Glucose Uptake and Insulin Sensitivity (2013) · cites this paper as [33]
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Jelenik, T., Rossmeisl, M., Kuda, O., Jilkova, Z. M., Medrikova, D., Kus, V., Hensler, M., Janovska, P., Miksik, I., Baranowski, M., et al. (2010) · Diabetes · doi:10.2337/db09-1716 · Cited by 88 · see citing works
Self-citationFrøsig, C., Pehmøller, C., Birk, J. B., Richter, E. A., & Wojtaszewski, J. F. P. (2010) · The Journal of Physiology · doi:10.1113/jphysiol.2010.194811 · Cited by 73 · see citing works
Self-citationAMPK activation regulates neuronal structure in developing hippocampal neurons
Ramamurthy, S., Chang, E., Cao, Y., Zhu, J., & Ronnett, G. V. (2014) · Neuroscience · doi:10.1016/j.neuroscience.2013.11.048 · Cited by 65 · see citing works
Metformin inhibits ROS production by human M2 macrophages via the activation of AMPK
Nassif, R. M., Chalhoub, E., Chedid, P., Hurtado-Nedelec, M., Raya, E., Dang, P. M.-C., Marie, J.-C., & El-Benna, J. (2022) · Biomedicines · doi:10.3390/biomedicines10020319 · Cited by 63 · see citing works
Lefort, N., St.-Amand, E., Morasse, S., Côté, C. H., & Marette, A. (2008) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.90362.2008 · Cited by 57 · see citing works
Potentiation of insulin-stimulated glucose transport by the AMP-activated protein kinase
Ju, J.-S., Gitcho, M. A., Casmaer, C. A., Patil, P. B., Han, D.-G., Spencer, S. A., & Fisher, J. S. (2007) · American Journal of Physiology-Cell Physiology · doi:10.1152/ajpcell.00269.2006 · Cited by 47 · see citing works
Deshmukh, A. S., Treebak, J. T., Long, Y. C., Viollet, B., Wojtaszewski, J. F. P., & Zierath, J. R. (2008) · Molecular Endocrinology · doi:10.1210/me.2007-0448 · Cited by 44 · see citing works
Self-citation
- Authors
- Viollet, B., Andreelli, F., Jørgensen, S. B., Perrin, C., Geloen, A., Flamez, D., Mu, J., Lenzner, C., Baud, O., Bennoun, M., Gomas, E., Nicolas, G., Wojtaszewski, J. F. P., Kahn, A., Carling, D., Schuit, F. C., Birnbaum, M. J., Richter, E. A., Burcelin, R., & Vaulont, S.
- Affiliations
- University of Copenhagen (DK)
- Centre National de la Recherche Scientifique (FR)
- Vrije Universiteit Brussel (BE)
- Howard Hughes Medical Institute (US)
- Hammersmith Hospital (GB)
- ORCID
- Venue
- Journal of Clinical Investigation
- Published
- 2003-01-01
- Volume
- 111
- Issue
- 1
- Pages
- 91-98
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC151837
- OpenAlex
- W2146027431
- Cited by
- 499
- References
- 40
- Citations by year
- 2026: 5 · 2025: 6 · 2024: 10 · 2023: 5 · 2022: 11 · 2021: 19 · 2020: 19 · 2019: 15 · 2018: 23 · 2017: 22 · 2016: 23 · 2015: 24 · 2014: 21 · 2013: 32 · 2012: 30
- FWCI
- 10.13
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Ghent University Academic Bibliography (Ghent University) (submittedVersion, other-oa)
- Research at the University of Copenhagen (University of Copenhagen) (submittedVersion)
- Funders
- Sundhed og Sygdom, Det Frie Forskningsråd
- European Commission
- National Research Foundation
- Institut National de la Santé et de la Recherche Médicale
- Danmarks Grundforskningsfond (504-12)
- Centre National de la Recherche Scientifique
- Medical Research Council
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Keywords
- AMPK, insulin sensitivity, insulin secretion, glucose metabolism, muscle glycogen synthesis, glucose transport, urinary catecholamine excretion, sympathetic nervous system, AMPK knockout mice, pancreatic islets
- MeSH terms
- Alleles, Animals, Biological Transport, Body Weight, Dose-Response Relationship, Drug, Genotype, Glucose, Glucose Tolerance Test, Glycogen, Insulin, Liver, Mice, Inbred C57BL, Multienzyme Complexes, Muscles, Time Factors, Blotting, Southern, Protein Serine-Threonine Kinases, Protein Structure, Tertiary, Mice, Knockout, Muscle, Skeletal, Catalytic Domain, Mice, AMP-Activated Protein Kinases
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
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