Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, USA.
Biochim Biophys Acta Mol Basis Dis. 2020 Oct 1;1866(10):165838. doi: 10.1016/j.bbadis.2020.165838. Epub 2020 May 16.
Metabolic syndrome is co-occurrence of obesity, insulin resistance, atherogenic dyslipidemia (high triglyceride, low high density lipoprotein cholesterol), and hypertension. It is a global health problem. An estimated 20%-30% of adults of the world have metabolic syndrome. Metabolic syndrome is associated with increased risk of type 2 diabetes mellitus, nonalcoholic fatty liver disease, myocardial infarction, and stroke. Thus, it is a major cause of morbidity and mortality worldwide. However, molecular pathogenesis of metabolic syndrome is not well known. Recently, there has been interest in the role of mitochondria in pathogenesis of metabolic problems such as obesity, metabolic syndrome, and type 2 diabetes mellitus. Mitochondrial dysfunction contributes to the oxidative stress and systemic inflammation seen in metabolic syndrome. Role of mitochondria in the pathogenesis of metabolic syndrome is intriguing but far from completely understood. However, a better understanding will be very rewarding as it may lead to novel approaches to control this major public health problem. This brief review explores pathogenesis of metabolic syndrome from a mitochondrial perspective.
代谢综合征是肥胖、胰岛素抵抗、动脉粥样硬化性血脂异常（高甘油三酯、低高密度脂蛋白胆固醇）和高血压的共同发生。它是一个全球性的健康问题。据估计，全世界有 20%-30%的成年人患有代谢综合征。代谢综合征与 2 型糖尿病、非酒精性脂肪性肝病、心肌梗死和中风的风险增加有关。因此，它是全球发病率和死亡率的主要原因。然而，代谢综合征的分子发病机制尚不清楚。最近，人们对线粒体在肥胖、代谢综合征和 2 型糖尿病等代谢问题发病机制中的作用产生了兴趣。线粒体功能障碍导致代谢综合征中所见的氧化应激和全身炎症。线粒体在代谢综合征发病机制中的作用很有趣，但远未完全了解。然而，更好地了解这一点将非常有意义，因为它可能为控制这一主要公共卫生问题提供新的方法。这篇简要综述从线粒体的角度探讨了代谢综合征的发病机制。
