Glycophagy is involved in cardiac glycogen regulation in response to exercise.
Autor: | James SL; Department of Physiology, University of Auckland, Auckland, New Zealand., Koutsifeli P; Department of Physiology, University of Auckland, Auckland, New Zealand., D'Souza RF; Department of Physiology, University of Auckland, Auckland, New Zealand., Masson SW; Department of Nutrition, University of Auckland, Auckland, New Zealand., Woodhead JS; Department of Nutrition, University of Auckland, Auckland, New Zealand., Merry TL; Department of Nutrition, University of Auckland, Auckland, New Zealand., Delbridge LM; Department of Anatomy and Physiology, University of Melbourne, Melbourne, Victoria, Australia., Mellor KM; Department of Physiology, University of Auckland, Auckland, New Zealand.; Department of Anatomy and Physiology, University of Melbourne, Melbourne, Victoria, Australia.; Auckland Bioengineering Institute, University of Auckland, Auckland, New Zealand. |
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Jazyk: | angličtina |
Zdroj: | Current research in physiology [Curr Res Physiol] 2024 Aug 23; Vol. 7, pp. 100131. Date of Electronic Publication: 2024 Aug 23 (Print Publication: 2024). |
DOI: | 10.1016/j.crphys.2024.100131 |
Abstrakt: | Cardiac glycogen-autophagy ('glycophagy') is disturbed in cardiometabolic pathologies. The physiological role of cardiac glycophagy is unclear. Exercise induces transient cardiac glycogen accumulation. Thus, this study experimentally examined glycophagy involvement during recovery from an exhaustive exercise protocol. Peak myocardial glycogen accumulation in mice was evident at 2 h post-exercise, preceded by transient activation of glycogen synthase. At 4 and 16 h post-exercise, glycogen degradation was associated with decreased STBD1 (glycophagy tagging protein) and increased GABARAPL1 (Atg8 protein), suggesting that glycophagy activity was increased. These findings provide the first evidence that glycophagy is involved in cardiac glycogen physiologic homeostasis post-exercise. Competing Interests: The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper. (© 2024 The Authors.) |
Databáze: | MEDLINE |
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