Cholecystokinin influences pancreatic trophism following total gastrectomy in rats

In rats, total gastrectomy (TG) has been shown to induce pancreatic hyperplasia and increased tissue concentrations of pancreatic trypsin and amylase, whereas lipase concentration was decreased. We performed total gastrectomy with the additional insertion of a duodenal tube in 17 rats. A central venous catheter was placed after 3 wk. The control groups consisted of sham-operated rats with a gastrotomy plus duodenal tube and a group of rats with only a duodenal tube. The rats received meal stimulation with a 6 mL liquid diet (3 mL oil, 2 mL amino acid solution, and 1 mL glucose) via duodenal tube upon recuperation. Blood samples were taken before as well as 5, 15, 30, and 60 minutes after the meal and analyzed for insulin, pancreatic glucagon, gastrin, and CCK by specific RIA techniques. Glucose tolerance was found to be impaired after total gastrectomy. Though insulin release was delayed compared to the controls, the integrated postprandial output was unchanged. The pancreatic glucagon release after the meal increased 83% in TG rats, compared to control rats. The baseline and postprandial gastrin values diminished 70% compared to control animals. Neither group exhibited a postprandial increase in gastrin levels. TG led to an increased postprandial CCK output of 72% compared to controls. The trophic changes of rat exocrine pancreas following total gastrectomy, therefore, could be based on an elevated postprandial release of CCK.