5‐Hydroxytryptamine contributes significantly to a reflex pathway by which the duodenal mucosa protects itself from gastric acid injury

2006 ◽  
Vol 20 (14) ◽  
pp. 2486-2495 ◽  
Author(s):  
Anders J. Smith ◽  
Alfred E. Chappell ◽  
Andre G. Buret ◽  
Kim E. Barrett ◽  
Hui Dong
Keyword(s):  
Gastric Acid ◽  
Duodenal Mucosa ◽  
Reflex Pathway

scholarly journals Duodenal Bulb Mucosa with Hypertrophic Gastric Oxyntic Heterotopia in Patients with Zollinger Ellison Syndrome

2009 ◽  
Vol 2009 ◽  
pp. 1-6 ◽  
Author(s):  
Emil Kohan ◽  
David Oh ◽  
Hank Wang ◽  
Salar Hazany ◽  
Gordon Ohning ◽  
...  
Keyword(s):  
Gastric Mucosa ◽  
Gastric Acid ◽  
Duodenal Bulb ◽  
Duodenal Mucosa ◽  
Heterotopic Gastric Mucosa ◽  
Blue Staining ◽  
Surface Epithelium ◽  
The Novel ◽  
Zollinger Ellison Syndrome ◽  
Gastric Type

Objectives. Zollinger-Ellison Syndrome (ZES) results in hypersecretion of gastric acid (via gastrinoma) leading to peptic ulcers, diarrhea, and abdominal pain. We describe the novel discovery of hypertrophic, heterotopic gastric mucosa in the proximal duodenal bulb in patients with ZES, which we hypothesize results in an increased incidence of postbulbar ulcers in patients with ZES (a mechanism previously unreported). We determined the incidence of the novel finding of duodenal gastric oxyntic hypertrophic heterotopia (GOH) in patients with ZES. Methods. Seven patients with ZES were enrolled. The diagnosis of ZES was established by hypergastrinemia, gastric acid hypersecretion, and a positive secretin test or based on biopsy specimens (evaluated via tissue staining). Basal acid output (BAO) and baseline gastrin secretion were determined by established methods. Endoscopic examinations with methylene blue staining and biopsy of the gastric and duodenal mucosa were conducted in all patients every 3–6 months for an average of 5 years. Results. The duodenal mucosa demonstrated hypertrophic GOH in 5 out of 7 patients with ZES and an intact stomach and duodenum. Biopsies from the bowel mucosa demonstrated patchy replacement of surface epithelium by gastric-type epithelium with hypertrophic oxyntic glands in the lamina propria in 5 patients. Two of the patients had no evidence of GOH in the duodenal bulb. Patients with GOH had an average serum gastrin level of 1245 pg/mL and BAO of 2.92 mEq/hr versus 724 pg/mL and 0.8 mEq/hr in patients without GOH. Conclusions. This study demonstrated the presence of duodenal mucosa with GOH in 5 out of 7 patients with ZES and an intact stomach and duodenum. The presence of hypertrophic and heterotopic gastric mucosa is proposed to result from increased gastrin levels and may contribute to the increased incidence of postbulbar ulcers in these patients.

Mucosal Enzyme Activities, with Special Reference to Enzymes Implicated in Bicarbonate Secretion, in the Duodenum of Rats with Cysteamine-Induced Ulcers

1983 ◽  
Vol 64 (3) ◽  
pp. 341-347 ◽  
Author(s):  
Danny Stiel ◽  
Denver J. Murray ◽  
Timothy J. Peters
Keyword(s):  
Carbonic Anhydrase ◽  
Gastric Acid ◽  
Brush Border ◽  
Brush Border Membrane ◽  
Subcutaneous Administration ◽  
Duodenal Mucosa ◽  
Bicarbonate Secretion ◽  
Biochemical Basis ◽  
Gastric Acid Hypersecretion ◽  
Acid Hypersecretion

1. Duodenal mucosa was collected from control rats and from animals which had received cysteamine, cysteamine plus cimetidine or pentagastrin. Animals which received cysteamine with or without cimetidine developed acute duodenal ulcers. Cysteamine treatment resulted in gastric acid hypersecretion, which was largely abolished by concurrent cimetidine administration. 2. Activities of enzymes implicated in bicarbonate secretion, HCO−3-activated ATPase, carbonic anhydrase and Na+ + K+-activated ATPase, were measured in the duodenal mucosa of control rats and animals 24 h after subcutaneous administration of cysteamine. Assays of these enzymes in duodenal mucosal homogenates from animals with cysteamine-induced ulcers showed significant decreases in HCO−3-activated ATPase and carbonic anhydrase activities compared with controls. 3. Alkaline phosphatase activity also fell significantly in the cysteamine-treated animals, and possibly reflects the HCO−3-activated ATPase activity in the brush-border membrane. in contrast, activities of other marker enzymes from the brush-border membrane and from several intracellular organelles were unchanged, indicating an absence of gross organelle pathology in this experimental model. 4. Similar changes in enzyme activity were not caused by treatment with pentagastrin. Administration of cimetidine with the cysteamine did not protect the animals against ulceration, and the activity of HCO−3-activated ATPase was persistently decreased. However, the carbonic anhydrase activity was unaltered in this latter group, compared with controls. 5. These findings suggest that in cysteamine-induced duodenal ulceration both gastric acid hypersecretion and impaired duodenal resistance occurs. It is suggested that decreased activities of key enzymes implicated in HCO−3 secretion may reflect the biochemical basis for the decreased mucosal resistance.

Telomere shortening is associated with reduced duodenal HCO3−secretory but normal gastric acid secretory capacity in aging mice

2012 ◽  
Vol 303 (12) ◽  
pp. G1312-G1321 ◽  
Author(s):  
Biguang Tuo ◽  
Zhenyu Ju ◽  
Brigitte Riederer ◽  
Regina Engelhardt ◽  
Michael P. Manns ◽  
...  
Keyword(s):  
Duodenal Ulcer ◽  
Gastric Acid ◽  
Short Circuit ◽  
Duodenal Mucosa ◽  
Ulcer Formation ◽  
Wild Type ◽  
Double Knockout ◽  
Telomere Shortening ◽  
Genetic Ablation ◽  
Secretory Capacity

The incidence of duodenal ulcer, especially Helicobacter pylori-negative duodenal ulcer, strongly increases with age. In humans, telomere length shortening is considered to be one critical factor in cellular senescence and organ survival. In this study, we compared basal and stimulated gastric acid and duodenal HCO3−secretory rates in aged late-generation (G3) telomerase-deficient (mTERC−/−) mice, which are characterized by severe telomere dysfunction due to the inability to elongate telomeres during cell division. We found that basal and forskolin-stimulated HCO3−secretion and short-circuit current ( Isc) in isolated duodenal mucosa of G3mTERC−/−mice were markedly reduced compared with age-matched wild-type mice. In contrast, basal and forskolin-stimulated acid secretory rates in isolated G3mTERC−/−gastric mucosa were not significantly altered. Correspondingly, duodenal mucosa of G3mTERC−/−mice showed slimming and shortening of villi, whereas gastric mucosal histology was not significantly altered. However, the ratios of cystic fibrosis transmembrane conductance regulator (CFTR) and solute-linked carrier 26 gene family (Slc26a6) mRNA expression in relation to cytokeratin-18 were not altered in duodenal mucosa. The further knockout of p21, which is a downstream effector of telomere shortening-induced senescence, rescued villus atrophy of duodenal mucosa, and basal and forskolin-stimulated duodenal HCO3−secretion and Iscin mTERC−/−p21−/−double-knockout mice were not different from wild-type controls. In conclusion, genetic ablation of telomerase resulted in p21-dependent duodenal mucosal atrophy and reduced duodenal HCO3−secretory capacity, whereas gastric morphology and acid secretory function were preserved. This suggests that telomere shortening during aging may result in an imbalance between aggressive and protective secretions against duodenal mucosa and thus predispose to ulcer formation.

scholarly journals The Physiology of the Gastric Parietal Cell

2020 ◽  
Vol 100 (2) ◽  
pp. 573-602 ◽  
Author(s):  
Amy C. Engevik ◽  
Izumi Kaji ◽  
James R. Goldenring
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Parietal Cell ◽  
Duodenal Mucosa ◽  
Parietal Cells ◽  
Apical Surface ◽  
Cell Secretion ◽  
Gastric Parietal Cell ◽  
Glucagon Like Peptide 1

Parietal cells are responsible for gastric acid secretion, which aids in the digestion of food, absorption of minerals, and control of harmful bacteria. However, a fine balance of activators and inhibitors of parietal cell-mediated acid secretion is required to ensure proper digestion of food, while preventing damage to the gastric and duodenal mucosa. As a result, parietal cell secretion is highly regulated through numerous mechanisms including the vagus nerve, gastrin, histamine, ghrelin, somatostatin, glucagon-like peptide 1, and other agonists and antagonists. The tight regulation of parietal cells ensures the proper secretion of HCl. The H+-K+-ATPase enzyme expressed in parietal cells regulates the exchange of cytoplasmic H+ for extracellular K+. The H+ secreted into the gastric lumen by the H+-K+-ATPase combines with luminal Cl− to form gastric acid, HCl. Inhibition of the H+-K+-ATPase is the most efficacious method of preventing harmful gastric acid secretion. Proton pump inhibitors and potassium competitive acid blockers are widely used therapeutically to inhibit acid secretion. Stimulated delivery of the H+-K+-ATPase to the parietal cell apical surface requires the fusion of intracellular tubulovesicles with the overlying secretory canaliculus, a process that represents the most prominent example of apical membrane recycling. In addition to their unique ability to secrete gastric acid, parietal cells also play an important role in gastric mucosal homeostasis through the secretion of multiple growth factor molecules. The gastric parietal cell therefore plays multiple roles in gastric secretion and protection as well as coordination of physiological repair.

Gastric Acid Secretory Value of Different Foods

1960 ◽  
Vol 39 (1) ◽  
pp. 1-11 ◽  
Author(s):  
Suzanne Saint-Hilaire ◽  
Marjorie K. Lavers ◽  
Joseph Kennedy ◽  
Charles F. Code
Keyword(s):  
Gastric Acid
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