Gastric acid secretion

Hersey, S. J.; Sachs, George

doi:10.1152/physrev.1995.75.1.155

Cited by 313 publications

(215 citation statements)

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“…G astric acid production originates in the parietal cell through the coordinated operation of apical and basolateral membrane transport proteins (1)(2)(3)(4)(5)(6)(7)(8)(9). The apical secretory machinery includes the gastric H-K-ATPase, a chloride channel, and a K ϩ recycling pathway (1)(2)(3)(4)(5)(6)(7)(8)(9).…”

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confidence: 99%

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Deletion of the chloride transporter Slc26a9 causes loss of tubulovesicles in parietal cells and impairs acid secretion in the stomach

Song

Miller

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

125

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confidence: 99%

“…The apical secretory machinery includes the gastric H-K-ATPase, a chloride channel, and a K ϩ recycling pathway (1)(2)(3)(4)(5)(6)(7)(8)(9). Despite an essential role for the apical Cl Ϫ channel in gastric acid secretion, its molecular identity remains unknown.…”

mentioning

confidence: 99%

Deletion of the chloride transporter Slc26a9 causes loss of tubulovesicles in parietal cells and impairs acid secretion in the stomach

Song

Miller

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

125

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show abstract

“…The key elements included in the model are cells, hormones, cellular factors, neural stimuli, acid and gastric protective mechanisms. Implicit in the model is that the two major regions of the stomach perform different tasks; the antrum transduces chemical and physical information into the lumen through modulation of gastrin levels, ultimately regulating the appropriate responses in the corpus (Hersey and Sachs, 1995). An outline of the elements in the model follows; for further details see Joseph et al (2002).…”

Section: The Stomach Physiologymentioning

confidence: 99%

“…Food volume ranges between 0.0 and 1.0 l, with 1.5 l as the maximal volume of the stomach (see Appendix for equation and graph of the feeding function). The underlying principle is that food ingestion increases the volume of the luminal contents, promoting distension of the stomach (Hersey and Sachs, 1995). The stretching of the stomach walls stimulates mechanoreceptors, resulting in gastrin release (Konturek et al, 1982;Weigert et al, 1997).…”

Section: Neural Components Bicarbonate and Feeding Functionmentioning

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

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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.

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“…There is increasing evidence that the precursor forms and the end product have distinct biological activities mediated by different receptors (3,31). Gastrin amide is the major hormonal regulator of gastric acid secretion (13,36) and acts as a mitogen for normal gastric epithelium and some gastric cancer cell lines in vitro and in vivo (9,17,20). The cholecystokinin (CCK)-B/gastrin receptor, which mediates the acid-stimulatory and proliferative effects of gastrin amide is a member of a family of receptors with seven transmembrane segments (21,39).…”

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Metabolism of recombinant progastrin in sheep

Paterson

Baldwin

Shulkes

2002

American Journal of Physiology-Endocrinology and Metabolism

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Precursor forms of peptide hormones may be biologically active with effects distinct from the mature end product. Nonamidated progastrin-derived peptides stimulate growth of colonic epithelium and are elevated in the circulation of patients with colorectal carcinomas, whereas the amidated end product is the major regulator of gastric acidity. Using region-specific radioimmunoassays, we here compared the in vitro and in vivo metabolism of recombinant human progastrin-(6–80) and two other nonamidated gastrins, gastrin-17-Gly and Tyr70-progastrin-(71–80). Although progastrin-(6–80) was very stable in vitro, both progastrin-(6–80) and gastrin-17-Gly were degraded in vivo. The in vivo data were best fitted by a double-exponential decay curve, and the half-lives for progastrin-(6–80) ( t ½α = 5.1 ± 1.1, t ½β = 42 ± 11 min) were significantly ( P < 0.05) longer than for gastrin-17-Gly ( t ½α = 2.2 ± 0.6, t ½β = 13 ± 1 min). Tyr70-progastrin-(71–80) was degraded more rapidly. Comparison with amidated gastrins suggests that peptide length, rather than sequence, is the critical determinant of clearance. Progastrin has the clearance characteristics to be considered a circulating hormone.

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Gastric acid secretion

Cited by 313 publications

References 0 publications

Deletion of the chloride transporter Slc26a9 causes loss of tubulovesicles in parietal cells and impairs acid secretion in the stomach

Deletion of the chloride transporter Slc26a9 causes loss of tubulovesicles in parietal cells and impairs acid secretion in the stomach

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

Metabolism of recombinant progastrin in sheep

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