Oxidative Stress Responsible for Cellular Defects in Diabetes

MONDAY, Jan. 14 (HealthDay News) -- In mice, alterations in mitochondria occur only after the onset of diabetes and are due to the production of reactive oxygen species (ROS) by muscle. In addition, mitochondrial alterations can be reversed by treating with antioxidants or normalizing glycemia, according to the results of a study published online Jan. 10 in the Journal of Clinical Investigation.

Charlotte Bonnard, from Universite Lyon 1 in Lyon, France, and colleagues examined the structure and function of muscle mitochondria in mice during the development of insulin resistance and diabetes due to a high-fat, high-sucrose diet.

The researchers found that diabetes but not glucose intolerance was associated with alterations in mitochondrial biogenesis, structure and function. Diet-induced diabetic mice had increased production of ROS in skeletal muscle, and the ROS were associated with mitochondrial alterations. Muscle ROS fell and mitochondrial integrity was restored by antioxidant treatment or by normalizing glycemia.

"These data suggest that mitochondrial alterations do not precede the onset of insulin resistance and result from increased ROS production in muscle in diet-induced diabetic mice," Bonnard and colleagues conclude.

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