Studies on the mechanisms of food-stimulated gastric acid secretion in normal human subjects.

Abstract

A B S T R A C T Liquid test meals were infused into the stomach and acid secretion was measured by intragastric titration at pH 5.0. Acid secretion after 500 or 750-ml sodium chloride meals was two to three times higher than basal secretion rates and was equivalent to 25-30% of the peak acid output in response to histamine. Since these meals did not cause a rise in serum gastrin concentration, it is assumed that they stimulate acid secretion by causing distention of the body and fundus of the stomach. Compared with this distention stimulus, glucose meals had no effect on acid secretion and fatinhibited acid secretion; however, both glucose and fat caused an increase in serum gastrin concentration. Amino acids caused a much greater increase in serum gastrin concentration and enhanced acid secretion above that noted with distention alone. In contrast, albumin did not enhance the serum gastrin concentration or stimulate acid secretion to a statistically significant extent.There was a close correlation between the rise in serum gastrin concentration and rate of acid secretion after different test meals when average results for each test meal were plotted. However, there was a poor correlation between acid secretion and serum gastrin concentration when the responses of the individual subjects with a given test meal were compared.Our interpretations are: (a) Distention is an important stimulant of the acid-secretory response to a meal, and this is not mediated by gastrin release. (b) Gastrin is one but probably not the only mediator of the chemical phase of acid secretion, i.e., acid secretion noted with amino acids that cannot be explained by distention. (c) Glucose and fat also release gastrin; however, with

Ghrelin and gastric acid secretion

“…Among these, GRP has a stimulatory action on gastrin release from G cells [21] . Gastrin released by GRP stimulation is the most important physiological secretagogue and it has a primary role in postprandial acid secretion [22] . Gastrin stimulates acid secretion via enterochromaffin-like cells (ECL cell) [23] .…”

“…Gastrin is known to be released into the circulation in response to food [31] , and to play an important roles in increasing postprandial acid secretion [22] , and to exert activity on ECL cells [23] . It was shown that vagotomy did not affect the maximal response of acid secretion to gastrin administration thus indicating that the action of gastrin was not primarily dependent on vagal nerve [32] .…”

Gastric Acid Secretion is Abnormally Sensitive to Endogenous Gastrin Released after Peptone Test Meals in Duodenal Ulcer Patients

“…Once the menasurement of postprandial acid secretion in huma-n subjects became possible by the method of intragastric titration (3), attempts were made to correlate acid secretion with postprandial serumn gastrin concentrattioins, but no correlations were founld (3,4). This, however, is not unexpected, as these stuidies were based on the acid and gastrin responses to a single level of stimulation by a standard meal in different individuals.…”

Inhibiting gastric acid production does not affect intestinal calcium absorption in young, healthy individuals: A randomized, crossover, controlled clinical trial

“…fasting gastric pH values in healthy individuals are 1 to 3, and calcium is highly soluble in this environment. Because dietary protein is known to increase gastric acid secretion, (10)(11)(12) we decided to study the effect of a PPI in the setting of a highprotein diet, thereby maximizing gastric acid output. When acidic gastric chyme enters the duodenum, it stimulates secretin production, causing pancreatic and intestinal epithelial secretion of bicarbonate.…”

“…The study employed a crossover design in which each study subject served as his or her own control, thereby eliminating the confounding effect of interindividual variation on calcium absorption. We chose to use a high-protein diet for all interventions in our study because available data indicate that this would augment gastric acid production and intestinal calcium absorption, (10)(11)(12)(13) allowing us the best opportunity to quantify the contribution of gastric acid to calcium absorption.…”