Therefore, we conclude that regulation of miR-29-MCL-1 axis by insulin is a cardioprotective mechanism and compensatory hyperinsulinemia in conditions of hyperglycemia would regulate miR-29-MCL-1 axis in diabetic heart and prevent significant myocardial damage in young (11- and 15-week) ZDF rats. The gene discussed is MCL1; the disease is hyperinsulinism.