The incidence of type 2 diabetes in Western society is on the rise, due largely to an increasing prevalence of obesity.
Dysfunction of skeletal muscle mitochondria, the powerhouses of a cell, is associated with type 2 diabetes; however, whether this association is causal or consequential has not been understood.
A new study by Jennifer Rieusset and her colleagues at INSERM U870, France, has shed light on this question and has provided evidence that alterations in mitochondrial function are the result, and not the cause, of insulin resistance (which usually precedes full-blown clinical type 2 diabetes) in mice.
Mice fed a high-fat, high-sucrose diet (HFHSD) developed insulin resistance and type 2 diabetes. The authors found that mitochondrial defects were present in diabetic, but not pre-diabetic glucose intolerant, mice.
The mitochondrial disruptions were subsequently shown to be the result of the generation of reactive oxygen species (ROS), highly reactive molecules implicated in a number of cellular disruptions. Indeed, ROS production coincided with mitochondrial dysfunction, and antioxidant treatment blocked the mitochondrial alterations in muscle cells.
The authors therefore concluded that treatment of diabetics with medications that either block ROS production or counteract their deleterious effects might improve the success of conventional therapies.
Journal article: Mitochondrial dysfunction results from oxidative stress in the skeletal muscle of diet-induced insulin-resistant mice. Journal Of Clinical Investigation. January 10, 2008.
Materials provided by Journal of Clinical Investigation. Note: Content may be edited for style and length.
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