The hypothesis appeared to be supported by animal studies in which intracerebral administration of leptin suppressed feeding and caused weight loss, and by the similar efficacy of leptin administration to reduce appetite and obesity in children [34] and rodents [35] rendered obese by the genetic loss of capacity to secrete leptin, but not in animals unable to express leptin receptor [36]. The gene discussed is LEP; the disease is obesity due to melanocortin 4 receptor deficiency.