sincalide and Hepatolenticular-Degeneration

The objectives of this study were (1) to examine basal and cholecystokinin-stimulated pancreaticobiliary secretion of zinc in normal subjects with zinc-adequate and zinc-deficient diets, and (2) to investigate whether basal and stimulated secretion of zinc was abnormal in patients with Wilson's disease before and after zinc therapy. Gastroduodenal intubation was performed in six healthy subjects and five patients with Wilson's disease. After intravenous infusion of octapeptide of cholecystokinin (40 ng/kg/hr) the pancreaticobiliary secretion of zinc increased from a basal rate of 283.1 +/- 75.8 nmol/L/min to a peak of 716.6 +/- 175.3 nmol/L/min in normal subjects. Normal subjects with a zinc-deficient diet had both lower basal (66.8 +/- 15.8 nmol/L/min) and stimulated (559.5 +/- 31 nmol/L/min) pancreaticobiliary secretion of zinc than with a zinc-sufficient diet. In contrast to the markedly reduced pancreaticobiliary secretion of copper, patients with Wilson's disease not treated with zinc had normal basal (226.6 +/- 126 nmol/L/min) and stimulated (728.7 +/- 195.5 nmol/L/min) zinc secretion. These studies indicate that a considerable amount of zinc is being secreted in pancreaticobiliary fluid in healthy subjects and there was no impairment of zinc secretion in patients with Wilson's disease. Our data also indicate that pancreaticobiliary secretion of zinc is dependent on the zinc status of the subjects, suggesting that endogenous secretion of zinc may play a significant role in the homeostasis of zinc.

Topics: Acetates; Acetic Acid; Adolescent; Adult; Bile; Copper; Diet; Hepatolenticular Degeneration; Humans; Male; Pancreas; Reference Values; Sincalide; Time Factors; Zinc