Sucrose nonfermenting AMPK-related kinase (SNARK) mediates contraction-stimulated glucose transport in mouse skeletal muscle
Open accessAbstract
The signaling mechanisms that mediate the important effects of contraction to increase glucose transport in skeletal muscle are not well understood, but are known to occur through an insulin-independent mechanism. Muscle-specific knockout of LKB1, an upstream kinase for AMPK and AMPK-related protein kinases, significantly inhibited contraction-stimulated glucose transport. This finding, in conjunction with previous studies of ablated AMPKα2 activity showing no effect on contraction-stimulated glucose transport, suggests that one or more AMPK-related protein kinases are important for this process. Muscle contraction increased sucrose nonfermenting AMPK-related kinase (SNARK) activity, an effect blunted in the muscle-specific LKB1 knockout mice. Expression of a mutant SNARK in mouse tibialis anterior muscle impaired contraction-stimulated, but not insulin-stimulated, glucose transport. Whole-body SNARK heterozygotic knockout mice also had impaired contraction-stimulated glucose transport in skeletal muscle, and knockdown of SNARK in C2C12 muscle cells impaired sorbitol-stimulated glucose transport. SNARK is activated by muscle contraction and is a unique mediator of contraction-stimulated glucose transport in skeletal muscle.
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The AMPK-related kinase SNARK is important for glucose uptake during contraction of mouse skeletal muscle.
“In addition to AMPK, the AMPK-related kinase SNARK has also been shown to be important for glucose uptake during contraction of mouse skeletal muscle [121].”
From AMPK and Exercise: Glucose Uptake and Insulin Sensitivity (2013) · cites this paper as [121]
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- Authors
- Koh, H.-J., Toyoda, T., Fujii, N., Jung, M. M., Rathod, A., Middelbeek, R. J.-W., Lessard, S. J., Treebak, J. T., Tsuchihara, K., Esumi, H., Richter, E. A., Wojtaszewski, J. F. P., Hirshman, M. F., & Goodyear, L. J.
- Affiliations
- Joslin Diabetes Center (US)
- Research Division, Joslin Diabetes Center and Department of Medicine, Harvard Medical School, Boston, MA 02215;
- University of Copenhagen (DK)
- National Cancer Center Hospital East (JP)
- ORCID
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2010-08-16
- Volume
- 107
- Issue
- 35
- Pages
- 15541-15546
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC2932588
- OpenAlex
- W2057374750
- Cited by
- 94
- References
- 46
- Citations by year
- 2025: 2 · 2024: 6 · 2023: 4 · 2022: 4 · 2021: 4 · 2020: 7 · 2019: 4 · 2018: 3 · 2017: 4 · 2016: 8 · 2015: 3 · 2014: 9 · 2013: 12 · 2012: 12
- FWCI
- 4.69
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Research at the University of Copenhagen (University of Copenhagen) (submittedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (DK36836, DK-68626, R01DK068626, P30DK036836, P30DK040561)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (AR45670, R01AR045670)
- 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
- snarks, AMPK-related kinases, skeletal muscle glucose transport, muscle contraction, LKB1, insulin-independent glucose transport, AMPKα2, tibialis anterior, C2C12 muscle cells, muscle-specific knockout mice
- MeSH terms
- Adult, Animals, Biological Transport, Cell Line, Enzyme Activation, Female, Glucose, Humans, Insulin, Male, Muscle Contraction, Phosphorylation, Physical Conditioning, Animal, Sorbitol, Blotting, Western, Exercise, Protein Serine-Threonine Kinases, Mice, Knockout, Muscle, Skeletal, Myoblasts, RNA Interference, Extracellular Signal-Regulated MAP Kinases, Mice, AMP-Activated Protein Kinases, In Vitro Techniques
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