Mice with genetic deletion of PPARγ in skeletal muscle showed significantly increased whole-body insulin resistance [59, 60, 100], demonstrated either by insulin/glucose tolerance tests or by hyperinsulinemic euglycemic clamp studies, and developed dyslipidaemia, enlarged fat pads, and obesity on high-fat diet [59, 60]. The gene discussed is INS; the disease is obesity due to melanocortin 4 receptor deficiency.