The relationship of intestinal fat to an augmented acid and gastrin response in dogs with a reversible pancreatic fistula

Abstract

Gastric hypersecretion results when pancreatic juices are excluded from the duodenum whether by pancreatic duct ligation, pancreatic fistula, pancreaticoileostomy, or pancreatectomy [l, 3-7,9, 10, 12, 13, 15, 21, 241. This phenomenon is well documented but the mechanism(s) have not been defined. A recent study from this laboratory indicates that in dogs with pancreatic duct ligation, an augmented antral gastrin response to meals was a primary factor in the induction of gastric hypersecretion (22). It was suggested that the augmented gastrin response resulted from an inadequate release of a fat-stimulated hormone that normally appears in response to a meal and that this hormone acts in part to inhibit mealstimulated gastrin release from the antrum. Investigations in the pancreatic duct-ligated animal model have inherent limitations [22]. This study investigates the gastrin and acid responses to meals in dogs with a reversible pancreatic fistula and the relationship of duodenal fat to these responses.