Moreover, specific gene ablation of the Lepr in a subset of hypothalamic neurons expressing nNOS results in hyperphagia, obesity, hyperglycemia, and decreased energy expenditure, suggesting that the leptin-induced inhibition of the NO synthesis in the brain is involved in determining its effects on the central regulation of feeding behavior [56] (Figure 1). The gene discussed is LEPR; the disease is obesity due to melanocortin 4 receptor deficiency.