The relationship between muscle mitochondrial nutritional overloading and insulin resistance
10.12701/yujm.2017.34.1.19
- Author:
Jae Han JEON
1
;
Jun Sung MOON
;
Kyu Chang WON
;
In Kyu LEE
Author Information
1. Department of Internal Medicine, Kyungpook National University School of Medicine, Daegu, Korea. leei@knu.ac.kr
- Publication Type:Review
- Keywords:
Insulin resistance;
Mitochondria;
Lipotoxicity;
Fatty acid oxidation;
Reactive oxygen species
- MeSH:
Adipose Tissue;
Diabetes Mellitus, Type 2;
Diet, High-Fat;
Incidence;
Insulin Resistance;
Insulin;
Liver;
Mitochondria;
Models, Animal;
Muscle, Skeletal;
Reactive Oxygen Species
- From:Yeungnam University Journal of Medicine
2017;34(1):19-28
- CountryRepublic of Korea
- Language:English
-
Abstract:
The incidence of type 2 diabetes mellitus and insulin resistance is growing rapidly. Multiple organs including the liver, skeletal muscle and adipose tissue control insulin sensitivity coordinately, but the mechanism of skeletal muscle insulin resistance has not yet been fully elucidated. However, there is a growing body of evidence that lipotoxicity induced by mitochondrial dysfunction in skeletal muscle is an important mediator of insulin resistance. However, some recent findings suggest that skeletal mitochondrial dysfunction generated by genetic manipulation is not always correlated with insulin resistance in animal models. A high fat diet can provoke insulin resistance despite a coordinate increase in skeletal muscle mitochondria, which implies that mitochondrial dysfunction is not mandatory in insulin resistance. Furthermore, incomplete fatty acid oxidation by excessive nutrition supply compared to mitochondrial demand can induce insulin resistance without preceding impairment of mitochondrial function. Taken together we suggested that skeletal muscle mitochondrial overloading, not mitochondrial dysfunction, plays a pivotal role in insulin resistance.
