Cited by 83Metabolism, Diabetes, and CancerAdipose Tissue and MetabolismMuscle Physiology and Disorders

Contraction-stimulated glucose transport in muscle is controlled by AMPK and mechanical stress but not sarcoplasmatic reticulum Ca2+ release

Open access
Jensen, Thomas E., Sylow, Lykke, Rose, Adam J., Madsen, Agnete B., Angin, Yeliz, Maarbjerg, Stine J., Richter, Erik A.·2014·Molecular Metabolism

Abstract

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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Crossref · 10.1016/j.molmet.2014.07.005

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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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Research works printed but not linked: 2

  1. [30]Li Q. Zhu X. Ishikura S. Zhang D. Gao J. Sun Y. Ca2+ signals promote GLUT4 exocytosis and reduce its endocytosis in muscle cells American Journal of Physiology. Endocrinology and Metabolism 307 2014 E209 E224 24895284
  2. [37]Witczak C.A. Jessen N. Warro D.M. Toyoda T. Fujii N. Anderson M.E. CaMKII regulates contraction-induced, but not insulin-induced, glucose uptake in mouse skeletal muscle American Journal of Physiology. Endocrinology and Metabolism 298 2010 E1150 E1160 20215576 PMC2886528

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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)
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
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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