Antral gastrin-producing G-cells and somatostatin-producing D-cells in different states of gastric acid secretion.

Abstract

SUMMARYThe number of G-and D-cells per area and the ratio of G/D-cells were investigated in biopsy specimens of the pyloric antrum from normochlorhydric subjects without peptic ulcer, from patients with duodenal ulcer, gastrinoma, pernicious anaemia, and after selective proximal vagotomy. Compared with normochlorhydric subjects antral G-cell density was significantly raised in pernicious anaemia, unchanged in duodenal ulcer, and diminished in gastrinoma patients. After vagotomy G-cell density was found to be raised if compared with patients with duodenal ulcer. D-cell density was significantly increased in gastrinoma patients, unchanged in duodenal ulcer, and diminished in pernicious anaemia and after vagotomy. The G/D-cell ratio was increased in pernicious anaemia and after vagotomy, unchanged in duodenal ulcer, and decreased in gastrinoma patients. It is concluded that the antral pH governs the ratio of G-and D-cells. Therefore, the G/D-cell ratio increases in states of reduced acid secretion and decreases in massive hyperchlorhydria. Hypergastrinaemia as such does not affect the G/D-cell ratio.A physiological role of the somatostatin-producing D-cells in the gastric mucosa has not been established. Regulation of gastric acid secretion has been suggested, because exogenous somatostatin inhibits basal and stimulated gastric acid secretion' and somatostatin is released into veins draining the antrum and the fundus. (Regulatory Peptides 1980; suppl.

Long-Term Omeprazole Treatment in Man: Effects on Gastric Endocrine Cell Populations

“…a pronounced increase in G cell volume density combined with a decrease in D cell volume density and consequently a marked increase in the G/D cell ratio. These observa tions gave support to the hypothesis that the antral G/D cell ratio is governed by the intragastric pH [ 18]. Again, changes of that order of magnitude have not been observed in this study in humans.…”

“…Since the physiolog ical fasting serum gastrin levels in our radio immunoassay do not exceed 60 pg/ml, part of the gastrin concentration increase was caused by the 'preperiod' of unsuccessful ranitidine treatment [17], The hypergastrinaemia is believed to be due to a negative feedback mechanism between intragastric pH and antral gastrin cell activity [8,17,18]. The further increase in gastrin levels after initiation of omeprazole therapy is probably a consequence of the stronger and more per manent suppression of gastric acid secretion by the benzimidazole derivative in compari son to the H2 receptor antagonist [17,19].…”

Abnormal functional and morphological regulation of the gastric mucosa in histamine H2 receptor–deficient mice

“…Chronic application of acidinhibitory drugs elevates serum gastrin levels (14,16,30), and it has been suggested that the gastric pH influences the population of endocrine cells such as gastrinproducing G cells (30)(31)(32). The long-term elevation of gastric pH may increase G-cell density and then elevate serum gastrin levels.…”

Comparison of the Effects of Pantoprazole and Its Enantiomers on Gastric Acid, Mucus, and Mucosa as Well as Endocrine Cells

“…The increase in G cell volume density is explained by feedback regulation and the decreased intragastric acidity results in a decrease in D cell volume density, since D cell growth is dependent on the stimulation of gastric acidity. 21,22) In this study, long-term administration of PAN·Na did show a tendency to increase G cell volume density, serum gastrin levels, parietal cell volume density, or mucosal thickness in the antrum, or a tendency to decrease D cell volume density. However, the increases in G cell and parietal cell volume densities in rats fed lower concentrations of (-)-PAN·Na and (±)-PAN·Na were more obvious than in rats fed higher concentrations of (-)-PAN·Na and (±)-PAN·Na.…”