Diabetic Myopathy: current molecular understanding of this novel neuromuscular disorder

We propose a mechanistic model for the development of diabetic myopathy based on the human findings to date. This model suggests that repeated insulin injections in those with T1D leads to recurrent periods of intracellular hyperglycemia in myofibers. Resultant reductions in mitochondrial function lead to greater reliance on glycolytic metabolism and a concomitant shift in fiber type composition. Studies defining the scope and magnitude of diabetic myopathy and testing the veracity of this model are urgently needed in order to develop appropriate therapeutic strategies to maximize muscle health in those with T1D.