Although diabetes mellitus is characterized by an apparent abundance of substrate with increased circulating levels of both free fatty acids and glucose, the diabetic myocardium uses almost exclusively free fatty acids for the generation of ATP, and its metabolic flexibility is dramatically reduced.3 This arises due to the combination of reduced glucose uptake4 and increased fatty acid oxidation,5 which mediates an inhibition of PDH (pyruvate dehydrogenase) as described by the Randle cycle,6 resulting in a reduced efficiency of ATP production. This evidence concerns the gene PDP1 and diabetes mellitus.