The salient findings from our current study suggest that the PK2/PKR pathway plays a crucial role in the pathogenesis of DCM and that Met treatment prevents diabetes-induced glucose and lipid metabolism dysfunction, cardiomyocyte apoptosis, fibrosis, and cardiac insufficiency by stimulating PK2/PKR and the downstream AKT/GSK3β pathway. This evidence concerns the gene AKT1 and familial dilated cardiomyopathy.