Publications

Abstract

Insulin resistance is a key defect associated with obesity and type 2 diabetes. Although a number of different factors have been proposed to contribute to the development of insulin resistance, studies in humans and rodents indicate that excess accumulation of lipid in insulin-target tissues is strongly associated with impaired insulin action. In recent times, a number of investigations have reported that various markers of mitochondrial metabolism are impaired in skeletal muscle from insulin-resistant individuals. These findings have led to the theory that defective mitochondrial function is an important factor leading to inappropriate lipid accumulation and the development of insulin resistance. In this contribution, we: (1) review the latest literature supporting a role for dysregulated mitochondrial metabolism in the development of insulin resistance; (2) highlight several recent studies that call into question the cause and effect relationship between mitochondrial dysfunction and impaired insulin action; and (3) discuss whether targeting mitochondrial function is an effective strategy for the treatment of insulin resistance and type 2 diabetes.