PPARα and PPARδ drive distinctcardiac metabolic regulatory programs in mouse models of type 2 diabetes.Indeed, PPARδ activates, whereas PPARα represses, targets involved in thecellular glucose utilization, resulting in reciprocal effects on cellularglucose uptake through differential regulation of glucose transporter 4(GLU4/SLC2A4) transcription. This evidence concerns the gene PPARA and type 2 diabetes mellitus.