Adam and Findlay, using the ovine model of obesity, which was characterized by increased body weight (BW) and external adiposity score and relatively increased ‘bad’ (low-density lipoprotein—LDL) cholesterol concentrations in circulating plasma (Adam and Findlay, 2010), support the hypothesis that the loss of the anorectic properties of central leptin associated with obesity is attributable to a decreased efficiency of blood–brain leptin transport and not to leptin insensitivity within the hypothalamus. The gene discussed is LEP; the disease is obesity due to melanocortin 4 receptor deficiency.