Abstract：
Human skeletal muscle mitochondria regulate energy expenditure. Research has shown that the functionality of muscle mitochondria is altered in subjects with overweight, as well as in response to nutrient excess and calorie restriction. Two metabolic features of obesity and overweight are (1) incomplete muscular fatty acid oxidation and (2) increased circulating lactate levels. In this study, I propose that these metabolic disturbances may originate from a common source within the muscle mitochondrial electron transport system. Specifically, a reorganization of the supramolecular structure of the electron transport chain could facilitate the maintenance of readily accessible coenzyme Q pools, which are essential for metabolizing lipid substrates. This approach is expected to maintain effective electron transfer, provided that there is sufficient complex III to support the Q-cycle. Such an adaptation could enhance fatty acid oxidation and prevent mitochondrial overload, thereby reducing lactate production. These insights advance our understanding of the molecular mechanisms underpinning metabolic dysregulation in overweight states. This provides a basis for targeted interventions in the quest for metabolic health.
摘要：
人骨骼肌线粒体调节能量消耗。研究表明，超重受试者的肌肉线粒体功能发生了改变，以及对营养过剩和热量限制的反应。肥胖和超重的两个代谢特征是(1)肌肉脂肪酸氧化不完全和(2)循环乳酸水平升高。在这项研究中,我认为这些代谢紊乱可能源于肌肉线粒体电子传递系统中的共同来源。具体来说,电子传输链的超分子结构的重组可以促进容易接近的辅酶Q池的维持，这是代谢脂质底物所必需的。这种方法有望保持有效的电子转移，前提是有足够的复合物III来支持Q循环。这种适应可以增强脂肪酸氧化并防止线粒体过载，从而减少乳酸的产生。这些见解促进了我们对超重状态下代谢失调的分子机制的理解。这为寻求代谢健康的针对性干预提供了基础。
