Mitochondria are important for adenosine triphosphate (ATP) production, which is vital for all living organisms. Mitochondria are also the key regulator of glucose‐stimulated insulin secretion in the pancreatic β‐cells4. During the past two decades, a growing body of evidence has shown that mitochondrial function is closely related to various facets of diabetes – pancreatic β‐cell dysfunction, insulin resistance, obesity and vascular complications of diabetes. In the present article, we briefly review the mitochondrial metabolism and focus on the etiologies of mitochondrial dysfunction and its impact on T2DM.
Obesity
Industrialization and westernization have dramatically changed the Korean lifestyle. Koreans are constantly deprived of physical activity and oversupplied with calories. These have led to an explosion of the obesity epidemic worldwide. It is now well‐known that chronic aerobic exercise increases mitochondrial content in muscle, thereby increasing the ATP generating capacity52. On the contrary, chronic disuse of muscle decreases mitochondrial content and oxidative capacity leading to impaired glucose utilization53. In regard to energy intake, a chronic high fat diet leads to insulin resistance. In a recent report, it has been shown that a high fat diet leads to insulin resistance in rodents and humans mainly by increasing mitochondrial H2O2 generation54. Blocking H2O2 emission from mitochondria by targeting antioxidants to mitochondria or overexpressing catalase resulted in a marked reduction of insulin resistance in the high fat diet‐fed state54.
