Unlike the effect of PPARα on cardiac muscle, PPARαdeficiency had no significant effect on the responses of skeletalmuscle to either fasting or heavy exercise, perhaps due tocompensation by redundant functions of PPARδ [25].However, transgenic overexpression of PPARα in skeletalmuscle, using the muscle creatine kinase (MCK) promoter, protectedmice from HFD-induced obesity, albeit at the expense of glucoseintolerance and insulin resistance [26]. The gene discussed is INS; the disease is Obesity.