糖吞噬参与运动时的心糖原调节

IF 2.1 Q3 PHYSIOLOGY
Samuel L. James , Parisa Koutsifeli , Randall F. D'Souza , Stewart WC. Masson , Jonathan ST. Woodhead , Troy L. Merry , Lea MD. Delbridge , Kimberley M. Mellor
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引用次数: 0

摘要

心脏糖原自噬("glycophagy")在心脏代谢性疾病中会受到干扰。心糖原自噬的生理作用尚不清楚。运动会诱发短暂的心糖原累积。因此,本研究通过实验检测了在从剧烈运动方案中恢复时糖吞噬的参与情况。小鼠心肌糖原累积的峰值在运动后 2 小时明显出现,之前糖原合成酶被短暂激活。运动后4小时和16小时,糖原降解与STBD1(糖吞噬标记蛋白)的减少和GABARAPL1(Atg8蛋白)的增加有关,这表明糖吞噬活性增加了。这些发现首次证明了糖吞噬参与了运动后心肌糖原的生理平衡。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Glycophagy is involved in cardiac glycogen regulation in response to exercise

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.

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来源期刊
CiteScore
3.20
自引率
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审稿时长
62 days
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