James Samuel L, Koutsifeli Parisa, D'Souza Randall F, Masson Stewart Wc, Woodhead Jonathan St, Merry Troy L, Delbridge Lea Md, Mellor Kimberley M
Department of Physiology, University of Auckland, Auckland, New Zealand.
Department of Nutrition, University of Auckland, Auckland, New Zealand.
Curr Res Physiol. 2024 Aug 23;7:100131. doi: 10.1016/j.crphys.2024.100131. eCollection 2024.
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.
心脏糖原自噬(“糖噬”)在心脏代谢疾病中受到干扰。心脏糖噬的生理作用尚不清楚。运动可诱导心脏糖原短暂积累。因此,本研究通过实验检测了力竭运动方案恢复过程中糖噬的参与情况。小鼠心肌糖原积累峰值在运动后2小时明显出现,之前糖原合酶短暂激活。运动后4小时和16小时,糖原降解与STBD1(糖噬标记蛋白)减少和GABARAPL1(自噬相关蛋白8)增加有关,表明糖噬活性增加。这些发现首次证明糖噬参与运动后心脏糖原的生理稳态。