The inhibition of thermogenic program was likely due to hyperinsulinemia in these animals because it has previously been shown that inhibition of insulin secretion with diazoxide prevented the HFD-induced decrease in the expression of β3-adrenergic receptor, which is a potent stimulator of PGC-1α and UCP1 expression in brown fat [33]. The gene discussed is UCP1; the disease is hyperinsulinism.