Disease relevance of Gastrin-Secreting Cells

• Our data suggest that neither G-cell hyperplasia nor alterations in somatostatin release explain postvagotomy hypergastrinemia in the dog [1].
• Effect of Helicobacter pylori products and recombinant cytokines on gastrin release from cultured canine G cells [2].
• It was found that, although eradication of the H. pylori infection results in a dramatic reduction in stimulated gastrin secretion, it is not associated with a change in the numbers of antral G cells or D cells in patients with duodenal ulcer [3].
• Certain cytokines released in H. pylori gastritis, such as tumor necrosis factor alpha and specific products of H. pylori, such as ammonia, release gastrin from G cells and might be responsible [4].
• Intragastric balloons causing gastric hypertrophy, G-cell hyperplasia, and raised serum gastrin levels in rats [5].

High impact information on Gastrin-Secreting Cells

• Percutaneous transhepatic venous sampling of gastrin: value in sporadic and familial islet-cell tumors and G-cell hyperfunction [6].
• Gastric acid exerts a feedback inhibition on the secretion of gastrin from antral G cells [7].
• The aim of this study was to examine whether the cytokines tumor necrosis factor alpha or interleukin 8 (IL-8), which are produced in the gastric mucosa of patients with H. pylori-induced peptic disease or H. pylori products, can stimulate gastrin release from isolated cultured canine G cells [2].
• CONCLUSIONS: IL-8 stimulated gastrin release from isolated G cells, and the effect was potentiated by H. pylori products [2].
• We speculate that G cells express type I IL-1 receptors and TNF P55 but not TNF P75 receptors [8].

Chemical compound and disease context of Gastrin-Secreting Cells

• These observations suggest that enprostil may reduce G-cell hyperplasia and hypergastrinemia [9].
• The fasting serum gastrin concentrations were similar in all treatments, excluding one patient with antral G-cell hyperplasia; the postprandial gastrin responses were similarly higher with cimetidine and cimetidine plus pirenzepine than with pirenzepine [10].
• Mean tissue contents of PCr, ATP and glycogen (expressed as glucose) were 3.02, 2.47 and 5.07 micromol/g cell wt. in spontaneously active control muscles and 1.07, 1.65 and 1.83 after 20 min anoxia [11].
• The increase of G cells and the decrease of D cells is the consequence of achlorhydria achieved by very high omeprazole dosages and results in hypergastrinaemia [12].
• In rats, changes in gastric nerve fibers containing gastrin-releasing peptide (GRP) in cysteamine-induced duodenal ulcer were investigated in relation to the dynamics of gastrin-producing cells (G-cells) [13].

Biological context of Gastrin-Secreting Cells

• EGF receptor activation of primary cultures stimulated gastrin gene expression about twofold; whereas bombesin treatment of antral G cell cultures stimulated gastrin release but not gene expression [14].
• The secretory kinetics of the G cell in omeprazole-treated rats [15].
• Furthermore, the adenylate cyclase and phosphatidyl inositide second messenger systems seem to be intracellular mediators of gastrin secretion from human antral G cells [16].
• The gastrin peptide precursor synthesized in these RIN cell lines is subject to the same repertoire of posttranslational modifications within the cell's secretory apparatus (endoproteolytic cleavage, tyrosine sulfation, and C-terminal amidation) as seen in antral G cells [17].
• The correlation between the granule content of G cells and the antral content of gastrin suggests that hormone release occurs by exocytosis, rather than by any change in the content of individual granules [18].

Anatomical context of Gastrin-Secreting Cells

• We have presently investigated whether GABA also colocalizes with gastrin in G cells in rat antral mucosa [19].
• Immunocytochemical techniques using antigastrin antibody were employed to localize G cells in ectopic gastric mucosa of metaplastic and congenital origins and to compare their distribution with that in normal gastric mucosa [20].
• Also, the immunoreactivity of EGF receptors was observed in parietal cells and gastrin cells and faintly in surface epithelial cells and mucous neck cells of the proliferative zone [21].
• Destructive or stimulatory immune reactions, analogous to those seen in the thyroid gland, could affect the gastrin-secreting G cells and other paracrine cells [22].
• The peptide hormone gastrin is secreted from G cells of the gastric antrum and is the main inducer of gastric acid secretion via activation of its receptor the cholecystokinin 2 (CCK2) receptor [23].

Associations of Gastrin-Secreting Cells with chemical compounds

• Gastrin release from the antral gastrin-expressing cell (G cell) is regulated by bombesin and luminal factors [14].
• CONCLUSIONS: This is the first direct demonstration of GABA in gastrointestinal G cells [19].
• CONCLUSIONS: The effects of capsaicin-induced changes in antral D- and G-cell secretion and acetylcholine discharge are due primarily to release of CGRP [24].
• After PGE2 administration, no evidence of mucosal inflammation or atypia was observed, nor was there any evidence of ultrastructural changes in the overall appearance of the parietal and gastrin cells [25].
• Chronic exogenous high dose adrenal cortical steroid administration to dogs resulted in a 137% increase in G-cell mass with an associated enhancement of peak serum gastrin levels [26].

Gene context of Gastrin-Secreting Cells

• Bombesin dose-dependently increased gastrin secretion; this stimulatory effect on the G cell was significantly reduced after a 72-h starvation [27].
• In a functional assay, using the fluorescent multidrug resistance protein 1 substrate 5-carboxyfluorescein, an increased efflux activity of HT29(col) cells was measured, as compared to the wild-type HT29 G(+) cells [28].
• In normal tissues, VEGF immunoreactivity was detected in G cells and PP cells [29].
• Conversely, duodenal G-cells process progastrin to gastrin tetratriacontapeptide (G34-NH(2)) with little processing at Lys(74)Lys(75) [30].
• CONCLUSIONS: These data suggest that RUNX3 may play a physiologic role in chief cells and G cells in gastric mucosa, and that suppression of RUNX3 expression in intestinal metaplasia and carcinoma of human stomach may be implicated in gastric carcinogenesis [31].

Analytical, diagnostic and therapeutic context of Gastrin-Secreting Cells

• METHODS: Canine G cells were isolated by collagenase digestion, enriched by centrifugal elutriation, incubated with cytokines, bacterial components, or both, and gastrin release was measured by radioimmunoassay [2].
• Parietal and G cells, Ki67, TUNEL, villin and MUC2 expression were analysed by immunohistochemistry [32].
• Insulin was localized specifically to antral G cells of G-InsKi mice by double immunofluorescence staining using antibodies against insulin and gastrin [33].
• Gastrin plays a crucial role in the pathogenesis of hypergastrinaemic peptic ulcer disease, i.e. in the Zollinger-Ellison syndrome, antral G-cell hyperfunction and retained excluded antrum after subtotal gastrectomy [34].
• Following exposure of approximately 10(6) cells to 0.4 mM Cr(III) for 4 h, the Cr uptake by single cells was less than 10(-)(14) g/cell (as determined by GFAAS analysis and as confirmed by PIXE analysis where the Cr concentration was below the limit of detection) [35].

References