Metabolism of the NH2-Terminal Tridecapeptide of Gastrin-17 in Normal Subjects and Duodenal Ulcer Patients

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Abstract
The metabolism of the NH2-terminal tridecapeptide fragment of gastrin-17 ((1-13)G-17) was examined in normal subjects and duodenal ulcer patients. A dose of 65 pmol synthetic human (1-13)G-17/kg/h was infused intravenously for 90 min. After cessation of infusion the disappearance curve was similar in the two groups. The mean half-life, volume of distribution, and clearance rate were, for normal and duodenal ulcer subjects, 6.3 and 6.3 min, 100 and 93 ml/kg, and 11.0 and 10.2 ml/kg/h, respectively. The gastric acidity decreased during the infusion in duodenal ulcer patients (54 ± 11 to 40 ± 10 meq/l (p < 0.02)) but not in normal subjects. The results suggest that the increased serum concentrations of the NH2-terminal fragment of gastrin-17 in duodenal ulcer patients are not caused by a decreased metabolism of (1-13)G-17. Moreover, the data show that (1-13)G-17 reduces gastric acid secretion.