Carbohydrate and Fat Metabolism in Patients with Pheochromocytoma

Abstract

Abnormal carbohydrate metabolism in pheochromocytoma has been ascribed to glycogenolysis provoked by catecholamines. Studies in two patients with this tumor revealed two additional factors: suppression of insulin release and resistance to the hypoglycemic action of endogenous or exogenous insulin. Immediately after removal of the tumor, the response of plasma insulin levels to glucose and tolbutamide was exaggerated, but resistance to the hypoglycemic effects of insulin continued. These findings are attributed to concomitantly elevated plasma cortisol levels. With time, carbohydrate metabolism reverted toward normal. Before operation elevated fasting plasma free fatty acid levels (FFA) fell after oral glucose, whereas, unexpectedly, plasma glycerol levels did not. Both levels were reduced after exogenous insulin. In postoperative patients both plasma glycerol and FFA fell after glucose had been administered by mouth. Direct inhibition of lipolysis by insulin appeared decreased owing to both suppression of and resistance to this hormone during hypercatecholaminemia. Hyperglycemia enhanced re-esterification and regulated FFA, presumably thereby averting ketoacidosis.