Glucocorticoid excess can decrease glucose utilization, increase hepatic glucose production, and stimulate glucagon secretion, lipolysis, proteolysis, and gluconeogenesis. These hormones also exert a permissive effect on gluconeogenesis, glycogenolysis, and lipolysis. All of these effects are accentuated by insulin deficiency. Hypercortisolemia potentiates the actions of catecholamines and glucagon on glucose production. Glucocorticoids, as long as present in permissive amouts, appear to play a minimal role-if any-in acute glucose counterregulation but may be important in the development of stress-induced hyperglycemia.