Cholecystokinetic and Pancreozymic Effect of O-Sulfated Gastrin Compared With Nonsulfated Gastrin and Cholecystokinin

To assess whether sulfated gastrin contributes to the cholecystokinetic and pancreozymic activity of plasma in humans, 8 healthy subjects on separate days received a mixed meal, graded i.v. infusions of synthetic human tyrosine-O-sulfated gastrin 17 (10.9, 32.7, and 98.1 pmol/kg · h), which was compared with nonsulfated gastrin 17 (12.2, 36.6, and 109.8 pmol/kg · h) and O-sulfated cholecystokininoctapeptide (5.5, 16.5, and 49.5 pmol/kg · h). Gallbladder volumes were measured by ultrasonography, and the concentrations of gastrin and cholecystokinin in the circulation were determined by specific radioimmunoassays. Neither of the gastrins induced changes in gallbladder volume at serum concentrations occurring postprandially, whereas cholecystokinin-octapeptide produced a significant reduction in gallbladder volume even at a plasma cholecystokinin concentration lower than observed postprandially. Another 8 subjects received the same infusions in combination with a background infusion of synthetic secretin (0.3 CU/kg · h). Gastric and duodenal juice was continuously aspirated using a double-marker perfusion technique. Neither of the gastrins caused an increase in the output of amylase, lipase, trypsin, chymotrypsin, or bilirubin, but both induced a modest increase in the output of bicarbonate and duodenal juice, the former only significantly during infusion of sulfated gastrin 17. The output of all parameters was significantly elevated during all doses of cholecystokininoctapeptide. The results indicate that neither of the gastrins stimulates gallbladder contraction and pancreatic enzyme secretion in humans under physiologic conditions. However, gastrin may, like cholecystokinin, potentiate the effect of secretin on pancreatic secretion of juice and bicarbonate.