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Gastrin has been proposed as a trophic factor for the pancreas. Extensive small-bowel resection increased transiently plasma gastrin levels in the rat and produced pancreatic growth. This growth was characterized by an increased pancreatic weight, protein and DNA content, and the occurrence of mitotic figures in acinar cells. In order to determine if gastrin is implicated in pancreatic hyperplasia, we induced endogenous variations of gastrin 3 weeks before small-bowel resection or transection. Hypogastrinemia was produced by antrectomy and hypergastrinemia by vagotomy plus pyloroplasty. Pyloroplasty alone was without any effect. All gastric operations alone enhanced though not significantly the weight of the pancreas and its content in protein and DNA. When performed before intestinal resection, they did not modify the hyperplastic response of the pancreas to the resection. Our findings do not support the views that antral gastrin exerts a trophic action on the rat pancreas and that gastrin is implicated in postresectional hyperplasia of the gland.

This work investigates the effect, on the rat pancreas, of a chronic administration of bombesin in function of the dose and duration of treatment and examines whether this effect may be mediated by the release of endogenous gastrin or cholecystokinin. Bombesin, administered three times daily for 5 or 15 days, induced a marked increase in pancreatic weight, its protein, RNA and enzyme contents with the dose of 10 micrograms/kg body weight; the ratios of pancreatic weight, protein and RNA contents to DNA contents increased significantly after a 5 day treatment, suggesting cellular hypertrophy. Pancreatic DNA content was markedly enhanced after a 15 day treatment, suggesting cellular hyperplasia. Antrectomy decreased plasma gastrin levels, but did not alter the pancreatico-trophic action of a 10 micrograms/kg bombesin treatment for 5 days. Proglumide, an inhibitor of cholecystokinin and gastrin in the pancreas, did not affect the growth of the pancreas induced by a 10 micrograms/kg bombesin treatment for 5 days. It is concluded that chronic bombesin induces, in the rat pancreas, cellular hypertrophy or hyperplasia depending on the duration of treatment. Pancreatic hypertrophy is not mediated by the release of endogenous gastrin or cholecystokinin.