These homozygous mice are not obese (heterozygotes were mildly obese) and do not show impairment of glucose tolerance (heterozygotes were mildly glucose intolerant possibly as a result of their mild obesity) although they have POMC processing defects, hyperproinsulinaemia and a block on intestinal glucagon like peptide-1 and -2 production (Zhu et al. 2002b). The gene discussed is POMC; the disease is obesity due to melanocortin 4 receptor deficiency.