Stomach acidity is a critical feature of the digestive system, facilitating the breakdown of protein through the activation of the protease pepsin. Gastric acid is secreted by H+/K+ ATPase, the gastric proton pump. A previous study on Nile tilapia (Oreochromis niloticus) showed that inhibiting the production of stomach acid using the proton pump inhibitor omeprazole (omz), reduced growth that correlated with an acceleration of the rate of gastric emptying. This contrasts with omz exposure studies in mammals in which there is a delay in gastric emptying and no impact on growth. To understand the mechanism behind rapid rates of gastric emptying in tilapia; the role of cholecystokinin (CCK) was examined in this study. CCK controls the rate of gastric motility as it contracts the most anterior part of the intestine to delay gastric emptying, holding food so that it can correctly go through the digestive process. Post-prandial changes in tilapia fed a fixed ration of 2% body mass day-1 of pellets either with (25mg kg-1 d-1) omeprazole or without was examined. Omeprazole treatment replicated the decrease in gastric acid secretion (88-94%), increased gastric emptying and decreased specific growth rate (30%) previously observed. Significantly, it lowered circulating plasma CCK concentrations and lowered cck gene expression in the anterior intestine as well as cckb receptor (cckbr) levels in the stomach, which is associated with the binding of the CCK hormone and gastrin (responsible for stimulating gastric acid secretion and motility) hormone that stimulates acid secretion. Together these results suggest a reduced release of CCK that would explain the accelerated rate of stomach emptying seen in tilapia. The expression of additional genes was looked at to determine the differences between omz vs sham treatments. While the expression of growth hormone and pepsinogen genes showed statistically significant differences, other genes showed no differences. A feeding trial was conducted to observe whether fish on an omeprazole diet could compensate for their reduced growth with an increase in appetite and food intake. Instead, there was no increase in food intake in omeprazole fed fish compared to the sham, with no difference in expression of genes for hunger at the transcriptional level. My study observed the interactions of gastric acidification and its relationship to the endocrine system on a molecular level not only with CCK but other hormones and genes that are influenced by gastric acidification, bridging the gap in knowledge between the interaction of the endocrine systems with the stomach in a teleost species.
Rema Abutaha (Thu,) studied this question.