Center for Neurosciences and Cell Biology, Department of Life Sciences, University of Coimbra, Portugal.
Curr Drug Targets. 2011 Jun;12(6):872-8. doi: 10.2174/138945011795529056.
Insulin resistant individuals manifest multiple disturbances in free fatty acids metabolism and have excessive lipid accumulation in insulin-target tissues. A wide range of evidence suggests that defective muscle mitochondrial metabolism, and subsequent impaired ability to oxidize fatty acids, may be a causative factor in the accumulation of intramuscular lipid and the development of insulin resistance. Such mitochondrial dysfunction includes loss of mitochondria, defects in the mitochondrial OXPHOS system and decreased rate of ATP synthesis. Stimulation of mitochondrial biogenesis appears as a strategy for the clinical management of the metabolic syndrome, by enhancing mitochondrial activity and protecting the cell against the increased flux of reduced substrates to the electron transport chain and thus reducing metabolic inflammation.
胰岛素抵抗个体表现出多种游离脂肪酸代谢紊乱，并在胰岛素靶组织中有过多的脂质积累。大量证据表明，肌肉线粒体代谢缺陷，以及随后氧化脂肪酸的能力受损，可能是肌肉内脂质积累和胰岛素抵抗发展的一个原因。这种线粒体功能障碍包括线粒体丧失、线粒体 OXPHOS 系统缺陷和 ATP 合成速率降低。刺激线粒体生物发生似乎是一种通过增强线粒体活性和保护细胞免受还原底物向电子传递链增加通量的策略，从而减少代谢炎症，来管理代谢综合征的临床策略。
