At a molecular level, PPARα is thought to be a key mediator of these metabolic alterations, as both T1D and T2D lead to increases in myocardial PPARα expression, and cardiac-specific PPARα overexpressing mice exhibit a cardiac phenotype mimicking that seen in diabetic cardiomyopathy (Finck et al., 2002, 2003). This evidence concerns the gene PPARA and type 1 diabetes mellitus.