Defective Inhibition of Gastrin Release by Antral Distension in Duodenal Ulcer Patients

Abstract

The gastrin response to a low and a high dose of gastrin-releasing peptide infusion was studied in healthy volunteers and in patients with duodenal ulcer disease. In duodenal ulcer patients, the gastrin response was exaggerated. Cholinergic blockade did not change the gastrin release in healthy volunteers. Antrum distension during neutralization of the gastric lumen was unable to stimulate gastrin release, also under cholinergic blockade. However, in healthy volunteers distension of the antrum significantly inhibited the gastrin response to gastrin-releasing peptide infusion. This inhibitory influence was most pronounced in patients given the lower dose of the neuropeptide. Cholinergic blockade counteracted the inhibitory effect exerted by antral distension. On the other hand, antral distension did not alter the gastrin response to gastrin-releasing peptide in patients with duodenal ulcer disease. These results suggest an additional defective inhibitory mechanism in duodenal ulcer patients.

Pathogenesis and therapy of gastric and duodenal ulcer disease

“…Numerous dysregulations were identified including elevated serum pepsinogen levels; elevated meal-stimulated gastrin secretion; and defective reflex inhibition of acid secretion induced by antral acidification, gastric distention, intraduodenal fat, or fasting [15][16][17][18]. Abnormalities in duodenal motility and bicarbonate secretion were also identified.…”

Helicobacter pylori and gut hormones

“…Acid secretion is normally inhibited by a low intragastric pH, but acid inhibition induced by peptones, intraduodenal fat, or gastric distension is attenuated in DU patients. [11][12][13] Meal-stimulated gastrin release is considerably greater in DU patients than in controls.…”

Pathogenesis of duodenal ulcer disease: the rest of the story

“…41 They found that the inhibitory eect on acid secretion induced by antral distention was restored after the H. pylori infection was cured, the eect being independent of whether duodenal ulcer disease was present. 41 None of the physiological alterations that appeared to be related to duodenal ulcer ± for example elevated serum pepsinogen levels, a defective re¯ex inhibition of acid secretion with antral acidi®cation 42 or gastric distention 43 , intraduodenal fat 44 , fasting 38 , an exaggerated gastrin response to meals or to the infusion of bombesin or GRP, an exaggerated acid output in response to meals or in response to bombesin or GRP infusion, and an exaggerated acid output in response to the instillation of acid ± have been proved to be more than reversible epiphenomena related to the H. pylori infection. 37 …”