DUODENAL ACIDIFICATION AND SECRETIN, BUT NOT INTRADUODENAL FAT, INHIBIT HUMAN GASTRIC-ACID SECRETION VIA PROSTAGLANDINS

Citation
Sd. Taylor et al., DUODENAL ACIDIFICATION AND SECRETIN, BUT NOT INTRADUODENAL FAT, INHIBIT HUMAN GASTRIC-ACID SECRETION VIA PROSTAGLANDINS, Gastroenterology, 107(6), 1994, pp. 1680-1685
Citations number
35
Categorie Soggetti
Gastroenterology & Hepatology
Journal title
ISSN journal
00165085
Volume
107
Issue
6
Year of publication
1994
Pages
1680 - 1685
Database
ISI
SICI code
0016-5085(1994)107:6<1680:DAASBN>2.0.ZU;2-R
Abstract
Background/Aims: Acid and fat in the duodenum inhibit gastric acid sec retion and increase plasma secretin. The role of prostaglandins and se cretin in the inhibition of gastric acid secretion by duodenal infusio n of hydrochloric acid and fat in healthy human volunteers was studied . Methods: Gastric acid secretion was submaximally stimulated with int ravenous pentagastrin followed by duodenal infusion of 0.1N hydrochlor ic acid, oleic acid, or intravenous secretin. To inhibit endogenous pr ostaglandins, the protocol was then repeated after indomethacin treatm ent. Results: Duodenal fat infusion inhibited acid secretion 80% +/- 5 % and was unaffected by indomethacin treatment. Intraduodenal acidific ation inhibited acid secretion by 43% +/- 8% and was reduced by indome thacin treatment to 15% +/- 4% (P < 0.01). Similarly, intravenous secr etin inhibited acid secretion by 34% +/- 3%, which was decreased to 13 % +/- 6% by indomethacin treatment (P < 0.01). The increase in plasma secretin levels after intraduodenal hydrochloric acid treatment was si gnificantly greater than that observed with intravenous secretin or in troduodenal oleic acid treatment; all were within the physiological ra nge. Acid in the duodenum releases secretin, which inhibits gastric ac id secretion at least in part via prostaglandins. In contrast, fat in the duodenum strongly inhibits gastric acid secretion via a nonprostag landin pathway. Conclusions: Secretin is the predominant mediator for the inhibition of human gastric acid secretion induced by the presence of acid, but not fat, in the duodenum.