G cell population of the gastric antrum, plasma gastrin, and gastric acid secretion in patients with and without duodenal ulcer.

Abstract

SUMMARYEstimates of the G cell population were made in 24 resected human pyloric antra from counts of cells in multiple samples and from measurements of antral size. Measurements had been made previously in 20 subjects of acid output (basal and after pentagastrin) and in 10 subjects of plasma gastrin (basal and after insulin + bicarbonate). G cells were most dense near the pylorus, but their circumferential distribution was even. The G cell populations ranged from 8 to 15 (mean 10) million in four control patients and from 3 to 43 (mean 18) million in 15 patients with duodenal ulcer. Those with recurrent ulcer after vagotomy had either a low G cell count and incomplete vagotomy, or a high G cell count and apparently complete denervation. Two patients with hypergastrinaemia and duodenal ulcer had moderate (29 x 106) or marked (56 x 106) excesses of G cells. 'G cell hyperplasia' may represent the extreme end of the normal range of G cell numbers in the antrum, and can be assessed by semi-quantitative grading of G cell hyperplasia in antral biopsies. There were significant direct correlations between antral area and G cell density, between peak acid output and G cell population, and between basal plasma gastrin and G cell density (but not population). We suggest that, in patients with duodenal ulcer, acid and gastrin secretion are interrelated and that both are related to the masses of parietal cells and of G cells.In 1967 Solcia and his colleagues described some endocrine-like cells in the gastric antrum which were argyrophilic, but non-argentaffin, in quality. The next year McGuigan (1968)

Pyloric Antrum Gastrin Cell Hyperplasia after Jejunum or Colon Transposition: Effects of Jejunal or Colonic Mucosa on G Cells

“…The en larged G cell mass [22], together with chronic basal stimulation by alkaline colonic mucins, could explain the observed hypergastrinemia. Unexpectedly, when serum gas trin was measured in freely fed animals, only a tendency towards increased values was found.…”

“…These findings favor the view that the transposed colonic mucosa produces some factor apt to induce G cell prolifera tion. Such a factor might involve hypersecre tion of alkaline fluids and viscous mucus which is known to occur following exposure of the colon to irritating agents [22],…”

The importance of an inter-compartmental delay in a model for human gastric acid secretion

“…Overall these findings lead us to suggest that an intrinsic inter-compartmental delay in gastrin transport is important in maintaining acid homeostasis. (Royston et al, 1978), 15.5 × 10 6 (dogs) (Nomiyama et al, 1981), 16.6 × 10 6 (dogs) (Takahashi et al, 1979) Antral D cells 3.70 × 10 6 9.53 × 10 6 ± 5.77 × 10 6 G/D cells ratio of 2 : 1 (Solcia et al, 1986), 11 × 10 6 (dogs) (Nomiyama et al, 1981) ECL cells 8.68 × 10 8 NA 30% total endocrine cell population (humans) (Helander et al, 1992); (D'Adda et al, 1989); 35% (Simonsson et al, 1988); 8.81 ×10 6 (rats)…”

Murine Models of Gastric Corpus Preneoplasia

“…Located in the antrum, G cells produce gastrin to both regulate gland homeostasis and promote acid secretion from parietal cells, primarily through the stimulation of histamine release from enterochromaffin-like cells 71, 72. Gastrin also functions as a growth factor for pit cells and exerts anti-apoptotic activity at the transcriptional level 73, 74, 75.…”