Inhibition of gastrin-stimulated gastric acid secretion by medium-chain triglycerides and long-chain triglycerides in healthy young men.

M.I.M. Maas, W.P.M. Hopman, M.B. Katan, J.B.M.J. Jansen

Research output: Contribution to journalArticleAcademicpeer-review

8 Citations (Scopus)

Abstract

Long-chain triglycerides inhibit gastric acid secretion, but the effect of medium-chain triglycerides in humans is unknown. We compared the effects of intraduodenally perfused saline, medium-chain and long-chain triglycerides on gastrin-stimulated gastric acid secretion and cholecystokinin release. Eight healthy male volunteers participated in this study. Gastrin-stimulated gastric acid output was 9.4 ± 1.1 mmol/30 min during saline perfusion. It was suppressed by medium-chain triglycerides by 43 ± 9% (P = 0.04 vs. saline) and by long-chain triglycerides by 74 ± 6% (P = 0.0003 vs. saline). Thus medium-chain triglycerides inhibited gastrin-stimulated gastric acid secretion but less so than long-chain triglycerides. When compared to saline perfusion (73 ± 6 pM x 30 min) integrated plasma cholecystokinin concentrations were significantly elevated by long-chain triglycerides (96 ± 5 pM x 30 min, P < 0.004) but not by medium-chain triglycerides perfusion (65 ± 7 pM x 30 min). We also investigated the role of cholecystokinin infusion on gastrin stimulated gastric acid secretion. Higher concentrations (191.4 ± 4.5 pM x 30 min) of CCK than released in the long-chain triglycerides perfusion experiment, did not suppress gastric acid secretion. Thus, circulating cholecystokinin appears not responsible for the inhibition of gastrin-stimulated gastric acid secretion by dietary fat.
Original languageEnglish
Pages (from-to)203-210
JournalRegulatory Peptides
Volume66
DOIs
Publication statusPublished - 1996

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