Mitochondrial dysfunction is the key detrimental factor in the development of acute insulin resistance Jiyun Ahn1, Hyunjung Lee1, Chang Hwa Jung1,2, Tae Youl Ha1,2, 1Korea Food Research Institute; 2University of Science and Technology
Insulin resistance (IR) is characterized by the failure of tissues to respond appropriately to insulin and contributes the important risk factor for type 2 diabetes, coronary heart disease and non-alcoholic fatty liver disease. Mitochondria play central roles in cellular energy metabolism and have been considered as a key contributor of metabolic disorder such as reduced ATP synthesis, ROS generation, and apoptotic cell death under high fat diet (HFD). However, there are still controversial for the role of mitochondria in the development of IR. Because mitochondrial dysfunction were not always observed in the IR. Therefore, to clarity the relationship between mitochondrial dysfunction and severity of IR, we compared the insulin sensitivity and mitochondrial functions in 2 weeks and 24 weeks-HF treated groups (HFD-S and HFD-L, respectively). 2 weeks of HFD significantly reduced mitochondrial content, citrate synthase activity and production of ATP. We observed decreased enzyme activity and protein expression of complex I in HFD-S mice. In addition, the transmission electron microscopy study showed noticeable decrease of the matrix density and loss of cristae structure in HFD-S mice. Western blot analysis of key components of the mitochondrial dynamics revealed the reduced fusion/fission mediators in HFD-S mice. These results demonstrated that mitochondrial function of skeletal muscle was damaged in the acute IR.
This work was supported by Korea Food Research Institute
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