This finds support in the results of investigation where the agonists of the types 3 and 4 melanocortin receptors (MC3R and MC4R) enhanced the ability of intracerebrally administered leptin to increase glucose utilization and to restore insulin sensitivity and lipid metabolism in mice with hyperglycemia, dyslipidemia and hyperinsulinemia, while their antagonists, on the contrary, prevented these effects of leptin [168]. The gene discussed is LEP; the disease is metabolic syndrome.