Mitochondrial dysfunction and insulin resistance: an update

被引:379
|
作者
Montgomery, Magdalene K. [1 ]
Turner, Nigel [1 ]
机构
[1] Univ New South Wales, Sch Med Sci, UNSW Med, Dept Pharmacol, Sydney, NSW 2052, Australia
基金
澳大利亚国家健康与医学研究理事会; 澳大利亚研究理事会; 英国医学研究理事会;
关键词
mitochondrial function; insulin resistance; lipid accumulation; oxidative stress; mitophagy; mitochondrial dynamics; HUMAN SKELETAL-MUSCLE; ACTIVATED PROTEIN-KINASE; FATTY-ACID OXIDATION; OXYGEN SPECIES PRODUCTION; ACETYL-COA CARBOXYLASE-2; RESPIRATORY COMPLEX-I; WEIGHT-LOSS; ENERGY-EXPENDITURE; METABOLIC SYNDROME; NONDIABETIC SUBJECTS;
D O I
10.1530/EC-14-0092
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Mitochondrial dysfunction has been implicated in the development of insulin resistance (IR); however, a large variety of association and intervention studies as well as genetic manipulations in rodents have reported contrasting results. Indeed, even 39 years after the first publication describing a relationship between IR and diminished mitochondrial function, it is still unclear whether a direct relationship exists, and more importantly if changes in mitochondrial capacity are a cause or consequence of IR. This review will take a journey through the past and summarise the debate about the occurrence of mitochondrial dysfunction and its possible role in causing decreased insulin action in obesity and type 2 diabetes. Evidence is presented from studies in various human populations, as well as rodents with genetic manipulations of pathways known to affect mitochondrial function and insulin action. Finally, we have discussed whether mitochondria are a potential target for the treatment of IR.
引用
收藏
页数:15
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