This may allow for a graded response to changing nutritional states, with acute changes in insulin acting via AgRP-dependent but melanocortin-independent pathways to affect BAT glucose uptake, and the sustained hyperglycemia and hyperinsulinemia accompanying more intense caloric intake additionally engaging the melanocortin circuit and the liver to allow for a concerted systemic response to lower postprandial blood glucose levels. The gene discussed is INS; the disease is Hyperinsulinemia.