The metabolic effects of VP are mediated via the V1a receptor (V1aR) and V1b receptor (V1bR) and include gluconeogenesis and glycogenolysis [28, 29], glucagon secretion [30], antilipolysis and hepatic production of triglycerides [31, 32], and adrenocorticotropic hormone (ACTH) release and hypercortisolism [33, 34]. The gene discussed is POMC; the disease is adrenal gland hyperfunction.