Recent studies suggest that
duodenal ulcers may develop because of increased drive to secrete
acid and decreased effectiveness of feedback mechanisms that inhibit
acid output. This study was designed to compare gastric acid,
gastrin, gastric inhibitory
peptide (GIP) and
secretin responses to meals (varying in pH) in 12 normal subjects and nine
duodenal ulcer patients.
Acid secretion was measured by an intragastric titration method which allows actual measurement of
acid response to food within the stomach (ten per cent
amino acid meal (AAM) adjusted to various pH levels, 7-1.5). Blood samples were collected at each pH level for radioimmunoassay of
gastrin,
secretin and GIP. Gastric acid and
gastrin responses to AAM were found to be significantly greater in
duodenal ulcer patients than in normal subjects. In
duodenal ulcer patients,
acid response to AAM at pH 7 or 5.5 reached 82% of
Histalog maximum. Decreasing the pH of the meal resulted in a stepwise reduction in both
acid secretion and
gastrin in normal subjects and
duodenal ulcer patients. At pH 1.5,
acid inhibition was complete, but
gastrin inhibition was partial.
Secretin increased significantly at pH 1.5; there was no difference in
secretin release between the groups. Plasma GIP was highest at pH 7 in all individuals. Use of a marker substance showed 80% recovery of AAM at pH 7-4; below pH 4, recovery rose to about 90%. We conclude that gastric acid and
gastrin release are pH-dependent in normal and
duodenal ulcer subjects. Inhibition of gastric secretion by acidified meals is associated with a pH-dependent suppession of
gastrin and GIP levels and elevation of plasma
secretin. This study confirms increased
acid and
gastrin responses in
duodenal ulcer patients but shows no evidence of defective feedback inhibition of gastric secretion and
gastrin release.