scholarly journals The prevalence and significance of circulating antibodies to gastric intrinsic factor and parietal cells in gastric carcinoma

Gut ◽  
1971 ◽  
Vol 12 (11) ◽  
pp. 903-905 ◽  
Author(s):  
B. Ungar ◽  
R. G. Strickland ◽  
C. M. Francis
2021 ◽  
Author(s):  
Wanjuan Wang ◽  
Ying Zhao ◽  
Zeqi Su ◽  
Fuhao Chu ◽  
Tao Li ◽  
...  

Abstract Background: Ethanol has been linked to atrophic gastritis and gastric carcinoma. Although it is well known that ethanol can result in hypochlorhydria, the molecular mechanisms underlying this phenomenon remain poorly understood.Results: Here we used gastric organoids to show that ethanol permeabilized the apical membrane of gastric parietal cells and induced ezrin hypochlorhydria. The functional consequences of ethanol on parietal cell physiology were studied using organoids. Gastric organoids were pre-incubated in the basic medium or with EGTA or E64 , and incubated at 37℃ in either medium alone, or medium containing 6% ethanol. We assessed ezrin proteolysis. Ethanol permeabilization induced activation of calpainⅠand subsequent proteolysis of ezrin, which resulted in the liberation of ezrin from the apical membrane of the parietal cells. Significantly, expression of calpain-resistant ezrin restored the functional activity of parietal cells in the presence of ethanol.Conclusion: Taken together, our data indicated that ethanol disrupted the apical membrane-cytoskeleton interactions in gastric parietal cells and thereby caused hypochlorhydria.


1992 ◽  
Vol 26 (10) ◽  
pp. 1283-1286 ◽  
Author(s):  
Rex W. Force ◽  
Milap C. Nahata

OBJECTIVE: To discuss the potential of histamine H2-receptor antagonists (H2RAs) to cause malabsorption of vitamin B12 (cyanocobalamin). DATA SOURCES: Pertinent literature was identified via a MEDLINE search. Journals and references cited in published articles also were used as data sources. STUDY SELECTION: Studies evaluating the effect of H2RAs on vitamin B12 absorption were reviewed. DATA SYNTHESIS: H2RAs decrease acid secretion by the gastric parietal cells. Gastric acid and pepsin produced by these cells are required for the cleavage of vitamin B12 from dietary sources. Intrinsic factor (IF), also produced by gastric parietal cells, is required for vitamin B12 absorption from the gastrointestinal tract. Although H2RAs have not conclusively been shown to decrease IF secretion, studies have demonstrated a significant reduction in food-bound vitamin B12 absorption secondary to decreased acid secretion in patients taking these drugs. CONCLUSIONS: H2RAs have the potential to cause vitamin B12 deficiency. This may be important in patients with inadequate stores of vitamin B12 (e.g., poor diet), particularly those receiving H2RA therapy continuously for more than two years. Healthcare providers should be aware of this potential adverse effect.


1998 ◽  
Vol 274 (1) ◽  
pp. G62-G70 ◽  
Author(s):  
J.-S. Shao ◽  
W. Schepp ◽  
D. H. Alpers

Morphological and functional heterogeneity of parietal cells has been thought to be due to different maturation positions within the gastric gland. Morphodynamic studies have shown that 2% of parietal cells in mice derive from a pre-neck (chief) cell precursor. Intrinsic factor (IF) and pepsinogen, markers of rat chief cells, were used to determine if these proteins identified a subset of parietal cells that might reflect origin from the pre-neck cell lineage. The zymogenic region of the rat stomach and gradient-isolated fractions enriched in parietal and chief cells were fixed in 10% buffered Formalin or in Bouin’s solution. Immunostaining was performed using indirect immunoperoxidase histochemistry and double-labeled immunofluorescence with antibodies raised against human IF, pepsinogen II, and H+-K+-adenosinetriphosphatase (H+-K+-ATPase). In intact tissue, parietal (H+-K+-ATPase-positive) cells were found starting at the upper edge of the isthmus, but parietal cells positive for IF and pepsinogen were only found from just below the isthmus and neck region to the base of the gastric gland. Three to four percent of isolated parietal cells were positive for these ectopic markers. This subset of cells was also positive for H+-K+-ATPase. Thus products of rat chief cells are expressed in a subset of parietal cells. The percentage of positive cells is similar to that predicted to be derived from the pre-neck (chief) precursor lineage in the mouse. The distribution of these cells to the lower neck and base of the gland suggests that the expression of chief cell products is consistent with either predetermination by lineage or parietal cell maturation or with both processes.


1990 ◽  
Vol 258 (3) ◽  
pp. G476-G483 ◽  
Author(s):  
J. J. Lewis ◽  
J. R. Goldenring ◽  
V. A. Asher ◽  
I. M. Modlin

The aim of this study was to elucidate the cellular mechanisms of action of epidermal growth factor (EGF) inhibition of parietal cell secretion. EGF effects on histamine- and carbachol-stimulated [14C]aminopyrine (AP) uptake and intrinsic factor (IF) secretion were evaluated in isolated rabbit parietal cells. EGF inhibited histamine-stimulated [14C]AP uptake and IF secretion through a reduction in stimulated adenosine 3',5'-cyclic monophosphate (cAMP) levels. EGF decreased the phosphorylation of a cytosolic 30-kDa, histamine-stimulated, cAMP-dependent protein kinase substrate. These effects on histamine-stimulated activation were reversed by pertussis toxin preincubation. EGF inhibited carbachol-stimulated [14C]AP uptake and IF secretion, but did not alter the carbachol-stimulated Ca2+ transient. These results indicate that EGF inhibits histamine-stimulated secretion through the inhibitory Gi guanosine 5'-triphosphate-binding protein and carbachol-stimulated secretion through a mechanism independent of the activation of an increase in intracellular Ca2+.


2020 ◽  
Vol 487 ◽  
pp. 112867
Author(s):  
Michaël V. Lukens ◽  
Carin A. Koelman ◽  
Joyce Curvers ◽  
Caroline Roozendaal ◽  
Liesbeth E. Bakker-Jonges ◽  
...  

1966 ◽  
Vol 4 (3) ◽  
pp. 11-12

In temperate climates deficiency of vitamin B12 is usually due to defective absorption, most commonly from lack of intrinsic factor as in Addisonian pernicious anaemia and after gastric surgery; occasionally the absorptive defect is caused by gastric carcinoma, resection, short-circuiting or disease of the ileum, including an abnormal bacterial flora, or by the fish tapeworm (Diphyllobothrium latum). The effectiveness of oral therapy remains debatable,1 and, since the absorptive defect can rarely be corrected, injections of vitamin B12 are virtually essential.


1985 ◽  
Vol 88 (5) ◽  
pp. 1132-1136 ◽  
Author(s):  
Joel S. Levine ◽  
Robert H. Allen

2020 ◽  
Author(s):  
Wanjuan Wang ◽  
Ying Zhao ◽  
Zeqi Su ◽  
Fuhao Chu ◽  
Tao Li ◽  
...  

Abstract Background: Ethanol have been linked to atrophic gastritis and gastric carcinoma. Although it is well known that ethanol can result in hypochlorhydria, the molecular mechanisms underlying this phenomenon remain poorly understood.Results: Here we used gastric organoids to show that ethanol permeabilized the apical membrane of gastric parietal cells and induced ezrin hypochlorhydria. The functional consequences of ethanol on parietal cell physiology were studied using organoids. Gastric organoids were pre-incubated in the basic medium or with EGTA or E64 , and incubated at 37℃ in either medium alone, or medium containing 6% ethanol. We assessed ezrin proteolysis. Ethanol permeabilization induced activation of calpainⅠand subsequent proteolysis of ezrin, which resulted in the liberation of ezrin from the apical membrane of the parietal cells. Significantly, expression of calpain-resistant ezrin restored the functional activity of parietal cells in the presence of ethanol.Conclusion: Taken together, our data indicated that ethanol disrupted the apical membrane-cytoskeletal interactions in gastric parietal cells and thereby caused hypochlorhydria.


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