Gastrin secretion from human antral G cells in culture

Campos, R. V.; Buchan, Alison; Meloche, R. M.; Pederson, Raymond A.; Kwok, Yin Nam; Coy, David H.

doi:10.1016/0016-5085(90)91226-v

Cited by 50 publications

(31 citation statements)

References 13 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…G cells are stimulated by gastrin-releasing peptide (GRP)/bombesin (1)(2)(3). Sympathomimetics, acetylcholine, prostaglandin, adenosine, and somatostatin are other substances known to act through specific receptors on canine G cells (1,(4)(5)(6)(7). All these receptors belong to the superfamily of seven-transmembrane, G-protein-coupled receptors.…”

Section: Introductionmentioning

confidence: 99%

“…All these receptors belong to the superfamily of seven-transmembrane, G-protein-coupled receptors. Postreceptor activation of gastrin release has mainly been studied in canine and human G cells (1,6,8). The intracellular pathways known to be involved in gastrin release are to some extent cAMP dependent.…”

Section: Introductionmentioning

confidence: 99%

“…The intracellular pathways known to be involved in gastrin release are to some extent cAMP dependent. Forskolin stimulates adenyl cyclase and increases gastrin release from isolated human and canine G cells (1,3,6). Gastrin release is enhanced when the concentration of cytosolic calcium is increased by calcium ionophores (1,3,6).…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Bombesin-induced gastrin release from canine G cells is stimulated by Ca2+ but not by protein kinase C, and is enhanced by disruption of rho/cytoskeletal pathways.

Seensalu¹,

Avedian²,

Song³

et al. 1997

J. Clin. Invest.

View full text Add to dashboard Cite

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Bombesin-induced gastrin release from canine G cells is stimulated by Ca2+ but not by protein kinase C, and is enhanced by disruption of rho/cytoskeletal pathways.

Seensalu¹,

Avedian²,

Song³

et al. 1997

J. Clin. Invest.

View full text Add to dashboard Cite

“…G, D and ECL cells secrete effectors upon receiving appropriate stimuli. G cells in the antrum secrete gastrin, a positive regulator of gastric acid secretion, upon receipt of ENS and CNS stimuli (Blair et al, 1986;Lundell et al, 1987;Campos et al, 1990;Dockray, 1999). Secreted gastrin diffuses into the antral blood capillaries.…”

Section: Neural Components Bicarbonate and Feeding Functionmentioning

confidence: 99%

“…Maximal secretion rate of gastrin due to ENS stimulation per cell 6.28 × 10 −17 Holst et al (1987), Nishi et al (1985) and Campos et al (1990) …”

Section: Parametersmentioning

confidence: 99%

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

Marino

Ganguli

Joseph

et al. 2003

Bulletin of Mathematical Biology

View full text Add to dashboard Cite

In this work we re-examine an existing model of gastric acid secretion. The model is a 2-compartment model of the human stomach accounting for regions where relevant cells (D, G, ECL and parietal cells) and proteins and acid they secrete (somatostatin, gastrin, histamine, and gastric acid, respectively) are found. These proteins compose a positive and negative feedback system that controls the secretion of gastric acid by parietal cells. The original model consists of 18 ordinary differential equations and yields a stable 3-period limit cycle solution. We modify the existing model by introducing a delay into the system and assuming that the cell populations are in steady state over a short-time window (<300 h) and are able to reduce the system to an 8-equation delay differential equation model. In addition to demonstrating congruency between the two models, we also show that a similar stability is only reproducible when the delay in gastrin transport is approximately 30 min. This suggests that gastric acid secretion homeostasis likely depends strongly on the delay in gastrin transport from the antrum to the corpus.

show abstract

Effect of Long‐term Omeprazole Treatment on Antral G and D Cells in Children

Pashankar,

Israel,

Jevon

et al. 2001

J. pediatr. gastroenterol. nutr.

View full text Add to dashboard Cite

BackgroundLong‐term omeprazole therapy is associated with hypergastrinemia. In the antrum, gastrin secretion from G cells is inhibited in a paracrine manner by somatostatin secreted from D cells. Omeprazole may alter the ratio of G to D cells; however, there are limited data concerning such an effect in humans and none in children. The authors studied the effect of long‐term omeprazole therapy on antral G‐ and D‐cell numbers in children.MethodsSix children received omeprazole for 4 to 7 years for erosive reflux esophagitis. Endoscopic antral biopsy specimens obtained at baseline and at 1, 4, and 7 years of omeprazole administration were immunostained to assess G and D cell numbers per antral gland. The G‐ and D‐cell numbers were also assessed in an age‐matched control group consisting of 24 healthy children from six different age groups.ResultsThe mean G‐cell number per unit area showed a significant increase at 4 years (85 ± 5.7 years) and at 7 years (89 ± 6.8 years) on omeprazole compared with baseline (56 ± 4.8 years) (P < 0.01). D‐cell numbers did not change. The ratio of G to D cells increased progressively, and the change from baseline was significant at 7 years taking omeprazole (P < 0.02). In the control group, G‐ and D‐cell numbers did not differ significantly within the six age groups.ConclusionsLong‐term omeprazole therapy is associated with a significant increase in G‐cell numbers and in the ratio of G to D cells in children. These changes reflect the effect of omeprazole because there was no change in these parameters in the age‐matched control group.

show abstract

Gastrin secretion from human antral G cells in culture

Cited by 50 publications

References 13 publications

Bombesin-induced gastrin release from canine G cells is stimulated by Ca2+ but not by protein kinase C, and is enhanced by disruption of rho/cytoskeletal pathways.

Bombesin-induced gastrin release from canine G cells is stimulated by Ca2+ but not by protein kinase C, and is enhanced by disruption of rho/cytoskeletal pathways.

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

Effect of Long‐term Omeprazole Treatment on Antral G and D Cells in Children

Contact Info

Product

Resources

About