Similar to our previous studies [13, 17], there were significant declines in both PPAR-α and PPAR-δ proteins and an increase in myocardial PPAR-γ protein levels in our DM hearts despite an increase in fatty acid oxidation, suggesting a compensatory response in preserving the contractile function induced by proinflammatory cytokines during hyperglycemia [44]. This evidence concerns the gene PPARD and diabetes mellitus.