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No evidence of direct association between GLUT4 and glycogen in human skeletal muscle

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posted on 2023-05-31, 05:41 authored by Robyn MurphyRobyn Murphy, M Flores-Opazo, Barnaby FrankishBarnaby Frankish, A Garnham, D Stapleton, M Hargreaves
Previous studies have demonstrated that exercise increases whole body and skeletal muscle insulin sensitivity that is linked with increased GLUT4 at the plasma membrane following insulin stimulation and associated with muscle glycogen depletion. To assess the potential direct association between muscle glycogen and GLUT4, seven untrained, male subjects exercised for 60 min at ~75% VO2 peak, with muscle samples obtained by percutaneous needle biopsy immediately before and after exercise. Exercise reduced muscle glycogen content by ~43%. An ultracentrifugation protocol resulted in a ~2-3-fold enriched glycogen fraction from muscle samples for analysis. Total GLUT4 content was unaltered by exercise and we were unable to detect any GLUT4 in glycogen fractions, either with or without amylase treatment. In skinned muscle fiber segments, there was very little, if any, GLUT4 detected in wash solutions, except following exposure to 1% Triton X-100. Amylase treatment of single fibers did not increase GLUT4 in the wash solution and there were no differences in GLUT4 content between fibers obtained before or after exercise for any of the wash treatments. Our results indicate no direct association between GLUT4 and glycogen in human skeletal muscle, before or after exercise, and suggest that alterations in GLUT4 translocation associated with exercise-induced muscle glycogen depletion are mediated via other mechanisms.

Funding

This study was supported by the Diabetes Australia Research Program and the National Health and Medical Research Council of Australia. Marcelo Flores-Opazo was supported by the Becas Chile scholarship program of CONYCIT.

History

Publication Date

2018-11-22

Journal

Physiological Reports

Volume

6

Issue

22

Article Number

e13917

Pagination

5p.

Publisher

Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society

ISSN

2051-817X

Rights Statement

© 2018 The Authors. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

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