Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01350 (gastrin)
 9,683 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Because of the unusual presentation of pernicious anemia in many black women, a further characterization of this disease among the different racial groups was undertaken. The following were found. (1) Black women under the age of 50 years had a significantly lower prevalence of anti-parietal cell antibody than did "European" and Latin-American patients or even older black women. The disease in the younger black women resembles juvenile pernicious anemia in this respect. Blacks in general had a lower prevalence of anti-parietal cell antibody than did "Europeans" and Latin Americans, though the difference was not statistically significant. A particularly striking finding was that anti-parietal cell antibody occurred much less often than anti-intrinsic factor antibody among black patients. (2) An analysis of all published HLA data for patients of European origin indicated a weak association of pernicious anemia with HLA-B7. However, no antigen association among the black and Latin-American patients studied was found. HLA-DR typing, not previously reported even for whites, also showed no association. (3) Lymphocytotoxic antibody was equally increased in frequency in all racial groups. (4) Serum gastrin levels did not follow a racial pattern; however, women with pernicious anemia had much higher levels than did men. (5) Pernicious anemia was not associated with blood group A.
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PMID:Profiles of black and Latin-American patients having pernicious anemia. HLA antigens, lymphocytotoxic antibody, anti-parietal cell antibody serum gastrin levels, and ABO blood groups. 721 50

22-Oxacalcitriol the analog with low calcemic effect and the original hormone 1,25(OH)2 vitamin D3 were localized by autoradiography in mouse stomach at different time intervals after intravenous injection. Both compounds showed a distinct nuclear concentration and retention in neck mucous cells of gastric and pyloric glands, and in dispersed endocrine cells in the antrum region. When the nuclear binding of radioactively labelled compound was compared between gastric neck cells and duodenal absorptive cells, binding was low but sustained in neck cells. Peak uptake after the injection was between 8 and 12 h in neck cells, but between 15 min and 30 min in duodenal villous epithelium. In the duodenum, weak nuclear labelling appeared at 8 h and was undetectable at 12 h under the conditions of the experiment. Nuclear labelling of neck cells remained detectable at 12 h and even after 24 h, similarly for both OCT and 1,25(OH)2 vitamin D3. These results suggest that the stomach is an important target tissue for vitamin D and its analog OCT. Regulation of neck cell functions is suggested, such as proliferation and differentiation of surface epithelium and gastric gland epithelium, and neck cell secretion of acidic mucus. Regulation is also indicated of G-cell gastrin secretion associated with gastrin paracrine effects on parietal cell HCl and intrinsic factor secretion, chief cell pepsinogen secretion, neck cell proliferation, as well as endocrine effects on systemic calcium homeostasis.
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PMID:Nuclear receptors for 1,25-dihydroxy-22-oxavitamin D3 (OCT) and 1,25-dihydroxyvitamin D3 in gastric gland neck mucous cells and gastrin enteroendocrine cells. 764 98

Twelve healthy volunteers (6 females, 6 males) between 26 and 36 years of age were enroled in this double-blind, randomized, placebo-controlled, three-way cross-over study. The objective was to determine the influence of lansoprazole (Agopton, Takeda Pharma GmbH, Aachen), a novel proton pump inhibitor, in doses of 30 and 60 mg, on the intragastric pH, on meal-stimulated gastric acid secretion and on the concentration of gastrointestinal hormones and enzymes in serum and gastric juice. Active drug or placebo had to be taken as single daily morning doses on an empty stomach for 7 days. Each wash-out period between drug application periods was 2 weeks long. Lansoprazole induced a dose-related increase in intragastric pH as well as a relevant reduction of basal acid output, meal-stimulated acid output and meal-stimulated secretion volume. 60 mg lansoprazole was significantly superior to 30 mg in increasing intragastric pH. The basal secretion volume in volunteers on 30 and 60 mg lansoprazole were lower than in volunteers on placebo. Serum gastrin and serum pepsinogen concentrations increased in a dose-dependent manner. Pepsin output and pepsin activity in gastric juice were slightly decreased in volunteers on 30 mg lansoprazole and markedly suppressed in volunteers on 60 mg lansoprazole 2 h after meal stimulation. Intrinsic factor concentration increased in volunteers on lansoprazole with a clear dose relationship. The evaluation of laboratory data and reported nonserious adverse events proved the relative safety of this new antiulcer agent.
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PMID:Influence of lansoprazole on intragastric 24-hour pH, meal-stimulated gastric acid secretion, and concentrations of gastrointestinal hormones and enzymes in serum and gastric juice in healthy volunteers. 775 Jun 67

Little data exist regarding the activity of gastric parietal and G cells in the very immature infant. Therefore, we have examined the developing human stomach for the presence and location of parietal and G cells, by using both standard histological methods and antibodies to the H+/K(+)-ATPase (proton pump), intrinsic factor and gastrin in 25 fetuses (ranging from 13-28 weeks) and in 5 infants (2-21 weeks). Parietal cell activity was noted in the body, antrum and pyloric regions in all the fetal specimens examined. However, this activity was much more limited in the infant specimens. Gastrin immunoreactivity was noted in all specimens from 18 weeks of gestation onwards; this activity was located solely in the antral and pyloric region. These results indicate that the human fetus has the potential to produce gastric acid, intrinsic factor and gastrin from the middle of the second trimester.
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PMID:When is the fetus first capable of gastric acid, intrinsic factor and gastrin secretion? 832 94

Achlorhydria that is due to antrum sparring atrophic gastritis is a characteristic finding in pernicious anemia. As a consequence of this achlorhydria serum gastrin level rise. Usually several signs are required for assessing a pernicious anemia: megaloblastic anemia, low serum cobalamin level, positivity of a Schilling test, low level of intrinsic factor in the gastric juice, existence of anti-intrinsic factor antibodies in plasma and/or in gastric juice. In this study the usefulness of the serum gastrin level is assessed. We report here the results in investigating sixteen patients with a pernicious anemia. All had: megaloblastic changes on bone marrow examination, serum cobalamin level lower than 150 pg/ml. For 14 patients the performed Schilling test was positive. For 2, no Schilling test was done, but anti-intrinsic factor antibodies were elevated. Serum gastrin levels were higher than 150 pg/ml (254 to 1770 pg/ml). In our patients with pernicious anemia, as a result of hypo or achlorhydria, serum gastrin increase was higher than in any other cause of hypochlorhydria: anti-acid treatment, vagotomy ... Measurement of serum gastrin is easy. High levels are simple to explain if found together with a sparing antrum atrophic gastritis and/or a low level of serum cobalamin. Serum gastrin measurement may be a cornerstone of rapid and reliable diagnosis of pernicious anemia.
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PMID:[The importance of hypergastrinemia in the diagnosis of Biermer's disease in the adult]. 844 53

Cobalamin (vitamin B12) is an essential nutrient derived exclusively from bacterial sources. It is an essential cofactor for three known enzymatic reactions. Untreated deficiency, caused by either the autoimmune disease pernicious anemia or nutritional lack, results in a macrocytic anemia and/or subacute combined degeneration of the spinal cord and is eventually fatal. Cobalamin in serum is bound to two proteins, transcobalamin and haptocorrin. The former is responsible for the essential delivery of cobalamin to most tissues. Inadequate tissue availability of cobalamin results in increased concentration of methylmalonic acid and homocyst(e)ine due to inhibition of methylmalonyl-CoA mutase and methionine synthase, respectively. Strict vegetarians have long been known to be at risk of cobalamin deficiency, which develops insidiously over many years. It is now clear that a significant number of the elderly and HIV-positive individuals are also at increased risk of deficiency. Any individual with reduced ability to split cobalamin from food-protein may also become deficient even though intrinsic factor is present. Diagnosis of cobalamin deficiency has frequently relied on total serum cobalamin and the Schilling test. Newer approaches such as analysis of methylmalonic acid, homocyst(e)ine, holotranscobalamin, anti-intrinsic factor antibodies, and serum gastrin may provide more cost-effective testing, as well as identify those with a covert deficiency.
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PMID:Cobalamin. 887 26

Autoantibodies arise when there is a breakdown in immunological tolerance. Autoantibodies to parietal cells and intrinsic factor are found in autoimmune atrophic gastritis (AAG) and are associated with elevated plasma gastrin. Endogenous gastrin autoantibodies have not been described to date. The aim of this study was to investigate the occurrence of autoantibodies to gastrin. Plasma from 50,000 patients, including more than 2000 with AAG, was tested. Gastrin was measured by radioimmunoassay (RIA) in whole plasma and the presence of autoantibody determined by using a control which omitted assay antibody. The quantity and affinity of gastrin autoantibodies was assessed. Three patients had autoantibodies to gastrin. All three had AAG and pernicious anaemia (PA). The antibodies were of low titre and relatively high affinity. Free circulating plasma gastrin levels were within the normal range, but total gastrin levels were elevated. This is the first description of autoantibodies to endogenous gastrin. The incidence of antibodies to gastrin is low, they are found in association with PA, and they may lead to falsely low measurements of plasma gastrin.
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PMID:Autoantibodies to gastrin in patients with pernicious anaemia--a novel antibody. 1002 36

To study in vivo the cellular differentiation and secretion of human developing fetal stomach, ethically and technically impossible to perform in utero, 256 fetal stomachs were xenografted. Human stomachs from 6- to 10-week-old fetuses were grafted for 1-273 days into nude mice. Biopsies for immunohistochemistry, hybridization and electron microscopy were taken and a catheter introduced into the human stomach. Macroscopic growth was fast and cells in S phase were numerous during the first 9 weeks, then the stomach size was stable and the gastric mucosa, of adult type, remained normal. In situ hybridization detected only a minute mouse mesenchymal chimerism in the graft. Chromogranin A, intrinsic factor and H+/K+ adenosine triphosphatase were immunohistolocally detected in epithelial cells 20 days after grafting, gastrin was detected after 30 days and pepsinogen after 60 days. The pH in gastric juice, which was at 8.0 +/- 0.1 from days 10-25, dropped from 4.39 +/- 1.80 at 30 days to 1.58 +/- 0.29 at 90 days. Intrinsic factor was stable and pepsin ranged from 6.8 +/- 7.8 to 134 +/- 51 units at 90 days. The differentiation of the epithelial cells in xenografts was very accelerated in comparison to that in utero.
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PMID:Morphologic and functional development of whole human fetal stomachs grafted into nude mice. 1147 49

Chronic inflammation of the gastric epithelium is believed to induce mucosal changes that can eventually develop into gastric cancer. In gastrin-deficient (G-/-) mice exhibiting chronic inflammation in the hypochlorhydric stomach, we documented a prominent fundic mucous cell lineage sharing morphological similarity with preneoplastic changes reported in Helicobacter-infected mice. To study the identity and origin of this cell lineage, we screened for different gastric mucosal cell markers. The clusters of large, foamy cells stained for trefoil factor 2 (TFF2/SP), MUC6 and the lectin Griffonia Simplicifolia II (GSII), but not for the intestine-specific transcription factor Cdx2, suggested that they arise from gastric mucous neck cells. Ki67-labeled GSII-positive neck cells in Helicobacter felis-infected, but not G-/- stomachs, suggested that mucous neck cell proliferation accounted for expansion of this compartment in the H. felis model of gastritis, but not the G-/- model. Using RNase protection assays and quantitative PCR, we found that interferon gamma (IFNgamma) was the most abundant proinflammatory cytokine in the G-/- stomach. We also found that this Th1 cytokine can increase the abundance of mucous neck cells, since its infusion into mice recapitulated the appearance of these cells as observed in both G-/- and H. felis-infected mice. Using the human gastric cell line NCI-N87, we showed that IFNgamma induces the secretion of mucus and expression of MUC6, TFF2 and pepsinogen II, but not of pepsinogen I and intrinsic factor. In conclusion, our results demonstrate that inflammation, specifically the proinflammatory cytokine IFNgamma, induced expansion of the fundic mucous neck cell compartment, which likely represents both increased mucus production and cell number.
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PMID:Interferon gamma induction of gastric mucous neck cell hypertrophy. 1576 19

Atrophic gastritis has been shown to involve either the oxyntic gland area, resulting in hypergastrinemia and hypopepsinogenemia I, the antral gland area, causing hypogastrinemia without change in serum pepsinogen I (diffuse antral gastritis; DAG), or the entire gastric mucosa (multifocal atrophic gastritis; MAG), resulting in both hypogastrinemia and hypopepsinogenemia I; and rare atrophic gastritis limited to the oxyntic gland area, with antibodies against oxyntic cells and/or intrinsic factor (autoimmune metaplastic atrophic gastritis; AMAG). This study was performed on 126 patients with various forms of gastritis and on 126 age- and gender-matched controls, who were subjected to endoscopy with biopsy, H. pylori testing (13C-UBT, serology), assays for serum gastrin and pepsinogen I, and testing for basal and pentagastrin-induced gastric acid secretion. The following groups of patients were examined: group I (N = 22), with AMAG; group II (N = 53), with DAG; group III (N = 51), with MAG; and group IV (N = 126), age- and gender-matched controls without gastritis. The following changes were found. In group I very high serum gastrin and very low pepsinogen I were observed, and all patients were achlorhydric and H. pylori negative. In group II, with low serum gastrin and normal pepsinogenemia and gastric chlorhydria, all patients were H. pylori positive. In group III, with lower serum gastrin and lower pepsinogen I levels and reduced chlorhydria, all patients were also H. pylori positive. And all group IV controls, with normal serum gastrin and pepsinogen I and normal gastric acid secretion without antral or fundic gastritis, were H. pylori negative. We conclude that measurements of serum gastrin and pepsinogen I and gastric acid secretion as well as testing for H. pylori infection may be useful in noninvasive diagnosis of various types of atrophic gastritis and in identification of patients with premalignant gastritis and a high risk of gastric cancerogenesis.
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PMID:Biomarkers in various types of atrophic gastritis and their diagnostic usefulness. 1581 Jun 29


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