Background: The present study was designed to investigate whether an effect of omeprazole on gastric emptying is related to changes in the secretion of selected gut hormones.
Methods: The studies were performed in healthy men after 10 days' treatment with 40 mg omeprazole daily/placebo. Food ingestion took place in a duodenal phase, I and the meal consisted of an omelette labelled with technetium Tc 99m, followed by 150 ml water labelled with indium In 111. Plasma concentrations of gastrin, cholecystokinin (CCK), and motilin were measured.
Results: Pretreatment with omeprazole reduced gastric emptying rates. This applied to all variables and was most pronounced with regard to amounts of solid (median (95% confidence interval)) emptied at 180 min (71% (48 - 86) for omeprazole versus 96% (87 - 100) for placebo; P < 0.01). All median values of plasma gastrin concentrations from the omeprazole series were higher than the corresponding values from the placebo series, and omeprazole induced a tenfold increase in incremental integrated area (IIA, pmol/l x 180 min) of the gastrin concentration curve (5250 (2570 - 9680) versus 575 (240 - 1485); P < 0.01). New findings include a lower postprandial secretion of CCK in the omeprazole series, and consequently, a difference in total integrated area (TIA, pmol/l x 180 min) (88 (21 - 147) versus 217 (104 - 267); P < 0.05) and IIA (pmol/l x 180 min) (52 (2 - 142) versus 165 (104 - 195); P < 0.05), respectively; a difference in IIA-30 (pmol/l x 30 min) of plasma motilin concentrations (270 (140 - 595) (omeprazole) versus 460 (285 - 655); P < 0.05); and a direct relationship between the amounts of liquid emptied at 30 min and the corresponding TIA-30 of plasma motilin in the omeprazole (Rs = 0.677; P < 0.05) and the placebo series (Rs = 0.767; P < 0.05).
Conclusion: Pretreatment with 40 mg omeprazole daily decreases the gastric emptying rates and has a substantial influence on the secretion of gastrin, motilin, and CCK. The finding of an omeprazole-induced decrease in CCK release may have clinical implications. Further investigation into the possible effect of proton-pump inhibitors on biliary tract motility and cholesterol solubilization in gallbladder bile is warranted.