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Measurement of Insulin- and Contraction-Stimulated Glucose Uptake in Isolated and Incubated Mature Skeletal Muscle from Mice
Published on: May 16, 2021
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Is contraction-stimulated glucose transport feedforward regulated by Ca2+?
Thomas E Jensen1, Yeliz Angin2, Lykke Sylow2
1Section of Molecular Physiology, Department of Nutrition, Exercise and Sports, University of Copenhagen, Denmark tejensen@nexs.ku.dk.
Experimental Physiology
|August 31, 2014
Summary
Sarcoplasmic reticulum calcium release does not directly regulate glucose transport in skeletal muscle. Instead, feedback signals from muscle contraction and mechanical stress are the primary drivers of glucose transporter activity.
Area of Science:
- Cellular physiology
- Muscle metabolism
- Signal transduction
Background:
- Calcium (Ca2+) signaling regulates vesicle transport in many cell types.
- Sarcoplasmic reticulum (SR) Ca2+ release initiates skeletal muscle contraction.
- SR Ca2+ release is traditionally thought to directly control glucose transporter 4 (GLUT4) translocation.
Purpose of the Study:
- To review evidence for the Ca2+ feedforward model of glucose transport regulation.
- To present findings challenging the direct role of SR Ca2+ release in muscle glucose transport.
- To propose an alternative model for contraction-stimulated glucose uptake.
Main Methods:
- Literature review of Ca2+ signaling and glucose transport.
- Analysis of experimental data on SR Ca2+ release and GLUT4 translocation.
- Development of a revised mechanistic model.
Main Results:
- Evidence supporting a direct Ca2+ feedforward role in glucose transport is re-evaluated.
- SR Ca2+ release is found to be neither essential nor adequate for stimulating muscle glucose transport.
- AMP-activated protein kinase (AMPK) and mechanical stress emerge as key feedback regulators.
Conclusions:
- The direct Ca2+ feedforward model for skeletal muscle glucose transport is not supported by current evidence.
- Contraction-stimulated glucose transport is primarily regulated by feedback mechanisms.
- A revised model emphasizes feedback signals from cross-bridge cycling and muscle tension.
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