Effect of fat on meal-stimulated duodenal acid load, duodenal pepsin load, and serum gastrin in duodenal ulcer and normal subjects

Abstract

We studied the effect of fat on meal-stimulated gastric acid and pepsin secretion, duodenal acid and pepsin load, and gastrin release in 10 duodenal ulcer (DU) patients and in 10 normal (N) subjects. Gastric acid and pepsin secretion and duodenal acid and pepsin load were measured at 20-min intervals for 140 min in response to two 500-ml equicaloric (400 kcal), equiosmolar (960 milliosmoles per liter), protein (10% w/v) meals; one meal also contained 22 g of fat (5% v/v), and the other contained 50 g of dextrose (10% w/v). Duodenal acid and pepsin load were determined by a serial dilution indicator method, which was validated in vitro and in vivo. The fat-containing meal produced significant inhibition of gastric acid and pepsin secretion and of duodenal acid and pepsin load in both the DU and N groups. The degree of inhibition of gastric acid secretion (50%), duodenal acid load (55%), gastric pepsin secretion (approximately 55%), and duodenal pepsin load (approximately 55%) did not differ significantly in the DU and N groups. The fat meal significantly inhibited gastrin release in the N subjects, but not in the DU patients. The acid and pepsin responses to the fat or carbohydrate meal were not significantly greater in the DU compared to the N group in spite of greater betazole- or pentagastrin-stimulated responses in the DU group. We conclude: (1) fat-induced inhibition of gastric acid and pepsin secretion and duodenal acid and pepsin load is not defective in DU patients; (2) however, the ability of fat to inhibit gastrin release does appear to be defective in DU patients; and (3) meal-stimulated acid and pepsin secretion was similar in both the DU and N groups.