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Yeungnam Univ J Med > Volume 34(1); 2017 > Article
Yeungnam University Journal of Medicine 2017;34(1):19-28.
DOI:    Published online June 30, 2017.
The relationship between muscle mitochondrial nutritional overloading and insulin resistance
Jae Han Jeon, Jun Sung Moon, Kyu Chang Won, In Kyu Lee
1Department of Internal Medicine, Kyungpook National University School of Medicine, Daegu, Korea.
2Department of Internal Medicine, Yeungnam University College of Medicine, Daegu, Korea.
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.
Key Words: Insulin resistance, Mitochondria, Lipotoxicity, Fatty acid oxidation, Reactive oxygen species


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