LKB1 and AMPK and the regulation of skeletal muscle metabolism
Open accessAbstract
PURPOSE OF REVIEW: To address the role of LKB1 and AMP-activated protein kinase (AMPK) in glucose transport, fatty acid oxidation, and metabolic adaptations in skeletal muscle. RECENT FINDINGS: Contraction-mediated skeletal muscle glucose transport is decreased in muscle-specific LKB1 knockout mice, but not in whole body AMPKalpha2 knockout mice or AMPKalpha2 inactive transgenic mice. Chronic activation of AMPK by 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR) and beta-guanadinopropionic acid enhances mitochondrial function in skeletal muscle, but AICAR or exercise-induced increases in mitochondrial markers are preserved in skeletal muscles from whole body AMPKalpha2 or muscle-specific LKB1 knockout mice. Pharmacological activation of AMPK increases glucose transport and fatty acid oxidation in skeletal muscle. Therefore, chronic activation of AMPK may be beneficial in the treatment of obesity and type 2 diabetes. SUMMARY: LKB1 and AMPK play important roles in regulating metabolism in resting and contracting skeletal muscle.
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AMPK detects the nutrient status of the cell and helps regulate glucose transport, fatty acid oxidation, and metabolic adaptations in skeletal muscle.
“Another enzyme central to cellular bioenergetics is AMP-activated protein kinase (AMPK), which detects the nutrient status of the cell and helps regulate glucose transport, fatty acid oxidation, and metabolic adaptations in skeletal muscle 159.”
From Cellular bioenergetics as a target for obesity therapy (2010) · cites this paper as [159]
Chronic activation of AMPK by AICAR enhances mitochondrial function in skeletal muscle.
“Chronic activation of AMPK by 5-aminoimidazole-4-carboxamide-1-β-D-ribofuranoside (AICAR, Table 2) enhances mitochondrial function in skeletal muscle 159.”
From Cellular bioenergetics as a target for obesity therapy (2010) · cites this paper as [159]
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O’Neill, B. T., Lauritzen, H. P. M. M., Hirshman, M. F., Smyth, G., Goodyear, L. J., & Kahn, C. R. (2015) · Cell Reports · doi:10.1016/j.celrep.2015.04.037 · Cited by 171 · see citing works
Self-citationKoh, 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., et al. (2010) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1008131107 · Cited by 94 · see citing works
Self-citationCandidate mechanisms accounting for effects of physical activity on breast carcinogenesis
Thompson, H. J., Jiang, W., & Zhu, Z. (2009) · IUBMB Life · doi:10.1002/iub.233 · Cited by 59 · see citing works
“Suppression is mediated through effects of PA on concentrations of the circulating growth factors and hormones that regulate the mTOR network but that are distinct from those affecting mTOR activity in contracting skeletal muscle as reviewed in (11, 12).”
Background
- Authors
- Koh, H.-J., Brandauer, J., & Goodyear, L. J.
- Affiliations
- Joslin Diabetes Center (US)
- Corresponding author
- Goodyear, Laurie J
- Venue
- Current Opinion in Clinical Nutrition and Metabolic Care
- Published
- 2008-05
- Volume
- 11
- Issue
- 3
- Pages
- 227-232
- ISSN
- 1363-1950 (ISSN-L)
- PMC
- PMC2887290
- OpenAlex
- W2036199274
- Cited by
- 78
- References
- 80
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 4 · 2023: 3 · 2022: 6 · 2021: 3 · 2020: 3 · 2019: 5 · 2018: 3 · 2017: 5 · 2016: 6 · 2015: 6 · 2014: 1 · 2013: 5 · 2012: 4
- FWCI
- 0.54
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Current Opinion in Clinical Nutrition & Metabolic Care (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (T32-DK-07260-29, DK-68626, R01DK068626, T32DK007260)
- 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
- LKB1, AMPK, skeletal muscle metabolism, glucose transport, fatty acid oxidation, mitochondrial function, muscle contraction, AMPKα2, AICAR, physical activity, obesity, type 2 diabetes
- MeSH terms
- AMP-Activated Protein Kinase Kinases, Animals, Enzyme Activation, Fatty Acids, Glucose, Humans, Multienzyme Complexes, Muscle Contraction, Protein Serine-Threonine Kinases, Mice, Knockout, Muscle, Skeletal, Mice, AMP-Activated Protein Kinases
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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.
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