Mice in which PPARβ/δ is selectively ablated inskeletal muscle myocytes exhibited a muscle fiber-type switching toward loweroxidative capacity that preceded the development of obesity and diabetes, thusdemonstrating that PPARβ/δ is instrumental in myocytes to maintenance ofoxidative fiber-type switching is likely to be the cause and not theconsequence of these metabolic disorders. The gene discussed is PPARD; the disease is obesity due to melanocortin 4 receptor deficiency.