These actions of the drug are complemented by activating the KATP channel in the dorsal motor nucleus of the vagus nerve (amplification of the effects of insulin, leptin and alpha-melanocyte stimulating hormone on pancreatic function, insulin resistance and satiety), pancreatic β-cells (reductions in hyperinsulinemia), and adipocytes (reduction in fatty acid biosynthesis and increased beta-oxidation of fat) to reduce hyperinsulinemia and accumulation of excess body fat, and to improve insulin and leptin resistance, and satiety [12]. Here, INS is linked to hyperinsulinism.