Contraction-stimulated glucose transport in muscle is controlled by AMPK and mechanical stress but not sarcoplasmatic reticulum Ca2+ release
Open accessAbstract
Understanding how muscle contraction orchestrates insulin-independent muscle glucose transport may enable development of hyperglycemia-treating drugs. The prevailing concept implicates Ca(2+) as a key feed forward regulator of glucose transport with secondary fine-tuning by metabolic feedback signals through proteins such as AMPK. Here, we demonstrate in incubated mouse muscle that Ca(2+) release is neither sufficient nor strictly necessary to increase glucose transport. Rather, the glucose transport response is associated with metabolic feedback signals through AMPK, and mechanical stress-activated signals. Furthermore, artificial stimulation of AMPK combined with passive stretch of muscle is additive and sufficient to elicit the full contraction glucose transport response. These results suggest that ATP-turnover and mechanical stress feedback are sufficient to fully increase glucose transport during muscle contraction, and call for a major reconsideration of the established Ca(2+) centric paradigm.
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Physical exercise increases skeletal muscle [18F]FDG uptake via GLUT4.
“Physical exercise increases skeletal muscle [18F]FDG uptake via GLUT4 [23].”
From Influences on PET Quantification and Interpretation (2022) · cites this paper as [23]
The Introduction (page unavailable) states that muscle contraction during exercise stimulates skeletal-muscle glucose uptake. The cited paper does not report [18F]FDG uptake or establish that the exercise-induced increase occurs via GLUT4; its GLUT4 discussion does not demonstrate that specific mechanism. (LLM, conf=0.88)
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- Authors
- Jensen, T. E., Sylow, L., Rose, A. J., Madsen, A. B., Angin, Y., Maarbjerg, S. J., & Richter, E. A.
- Affiliations
- University of Copenhagen (DK)
- Corresponding author
- Jensen, Thomas E.
- Venue
- Molecular Metabolism
- Publisher
- Elsevier BV
- Published
- 2014-10
- Volume
- 3
- Issue
- 7
- Pages
- 742-753
- ISSN
- 2212-8778 (ISSN-L)
- PMC
- PMC4209358
- OpenAlex
- W1991664482
- Cited by
- 83
- References
- 58
- Citations by year
- 2026: 4 · 2025: 5 · 2024: 4 · 2023: 2 · 2022: 7 · 2021: 8 · 2020: 9 · 2019: 13 · 2018: 5 · 2017: 9 · 2016: 8 · 2015: 5 · 2014: 4
- FWCI
- 3.56
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Molecular Metabolism (publishedVersion, cc-by-nc-nd)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Research at the University of Copenhagen (University of Copenhagen) (submittedVersion)
- Funders
- Natur og Univers, Det Frie Forskningsråd
- Københavns Universitet
- Lundbeckfonden
- Novo Nordisk Fonden
- Division of Earth Sciences
- 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
- muscle glucose transport, muscle contraction, AMPK, mechanical stress, sarcoplasmic reticulum Ca2+ release, insulin-independent glucose uptake, ATP turnover, passive muscle stretch, hyperglycemia
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