We speculate that peptide YY may play an important role in the inhibition of gastrin-stimulated gastric acid secretion by long-chain and medium-chain triglycerides.
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 m m ol/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.
Replacement of dietary lilt by sucrose polyester reduces fat intake. However, little is known about the effccts of sucrose polyester on gastrointestinal function. To investigate the effect on gastric acid secretion and on release of cholecystokinin into plasma, we perfused eight healthy male volunteers intraduodenally with sucrose polyester, digestible fat, or saline on separate days in random order, Intraduodenal perfusion of sucrose polyester did not suppress gastrin-stimulated gastric acid secretion ( -1.8 ± 6,8%) whereas digestible fat suppressed gastric acid secretion by 64 ± 9% (P = 0.001) compared with saline. Sucrose polyester did not affect plasma cholecystokinin concentrations (-12.8 ± 9.3 pmol • 30 min/L) whereas perfusion with digestible fat resulted in a significant increase (31.7 ± 9.3 pmol -30 min/L, P ~ 0,017) compared with saline. We conclude that sucrose polyester, in contrast with digestible fat, does not inhibit gastrin-stimulated gastric acid secretion or stimulate release of cholecystokinin,
KEY WORDS cholecystokininGastric acid secretion, sucrose polyester, Stimulation of plasma CCK and pancreaticobiliary secretion by fatty nutrients depends on the presence of the products of fat digestion in the proximal small intestine (23-29). The inhibi tion of gastric acid secretion by fat might dopend on (he digestion of fat as well.We report the effect of digestible fat and the indigestible fat sucrose polyester on gastric acid secretion and on CCK release in men.
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