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Mitochondrial dysfunction in metabolic syndrome

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ELSEVIER
DOI: 10.1016/j.bbadis.2020.165838

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Mitochondria; Obesity; Diabetes; Diabetes mellitus; Metabolic syndrome

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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.

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