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)

Hypersecretion of gastric acid, gastrin, and pepsinogen are considered to be causally related to duodenal ulcer diathesis. Until recently, these abnormalities have been considered to be primary and largely genetically determined. However, Helicobacter pylori infection has been shown to be responsible for several of the abnormalities of gastric secretion in duodenal ulcer. H. pylori infection is not only associated with chronic active inflammation but also with a reduction of somatostatin producing D-cells and somatostatin concentrations in the gastric mucosa. The reduced inhibitory action of somatostatin on the secretion of gastric acid, gastrin, and pepsinogen may be responsible for the hypersecretory state of the stomach in duodenal ulcer. These recent findings have drastically changed our understanding of the pathogenesis of duodenal ulcer.
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PMID:Gastric secretory abnormalities in duodenal ulcer: primary or secondary to Helicobacter pylori infection? 129 57

Elucidation of receptors and mediators regulating gastric pepsinogen secretion has lagged behind understanding of the factors that control acid secretion. During the past decade, as a consequence of the development of in vitro models for studying the control of pepsinogen secretion at the cellular level, much information about chief cell receptors and signal-transduction mechanisms has been obtained, including the identification and characterization of receptors for secretin, vasoactive intestinal polypeptide, cholinergic agonists, gastrin, cholecystokinin, peptide YY, and cholera toxin. Moreover, these cell preparations have permitted secretagogue-induced changes in chief-cell calcium concentration, protein kinase C distribution, and phosphoinositide and cyclic nucleotide content to be measured and related to changes in pepsinogen secretion. This article reviews these advances, discusses areas of uncertainty and controversy, and indicates areas for future investigation.
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PMID:Gastric chief cells: receptors and signal-transduction mechanisms. 131 85

Pepsinogen is an inactive precursor of pepsin, a typical aspartic proteinases, synthesized in the chief cells of gastric glands. There are two major groups of pepsinogen, namely pepsinogen A (PGA) and pepsinogen C (PGC) (or progastricsin), and each frequently has isozymogens. The relative extents of expression of the two pepsinogens vary among animal species and, moreover, their biosynthesis is known to be affected by such bioactive peptides as gastrin and secretin; however, the regulation mechanism of pepsinogen biosynthesis, hence pepsinogen gene expression is not yet clear. Therefore, it is thought to be of fundamental importance to elucidate the primary structures of the pepsinogen gene for such studies. This report describes the primary structures of human PGA and PGC genes and rat PGC gene. The organization of the genes is essentially the same; each gene was found to be separated into nine exons by eight introns of various lengths, encoding the amino acid sequence of the corresponding prepepsinogen. These results show that these genes are all derived from a common ancestral gene. The 5'-flanking region of human PGA gene, however, was different from those of human and rat PGC genes, whereas those of human and rat PGC genes were similar to each other. Thus, it is suggested that the expression of the PGA and PGC genes are somewhat differently regulated.
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PMID:Gene structures of pepsinogens A and C. 145 84

Effects of Ostertagia ostertagi infection on secretion of insulin, pancreatic glucagon, cortisol, gastrin, and pepsinogen were studied in calves inoculated with 100,000 (group 1) or 10,000 (group 2) O ostertagi infective larvae weekly for 14 weeks. Plasma insulin concentrations in both inoculated groups were lower than those in a non-infected (group 3) control group. The differences between group 1 and group 3 were significant (P < 0.05) at 2 and 12 weeks after initial inoculation. Plasma pancreatic glucagon and cortisol concentrations of groups 1 and 2 did not differ significantly from those of the control group, although plasma pancreatic glucagon concentration was consistently lower in group-1 calves from 4 weeks to end of the study. Plasma pepsinogen and serum gastrin concentrations also increased significantly (P < 0.05) in both groups that received inoculations. We concluded that decreased plasma insulin concentrations are contributory to changes in postabsorptive protein metabolism, and that serum gastrin concentrations are more representative of the pathologic changes in the abomasum than are plasma pepsinogen concentrations.
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PMID:Effects of Ostertagia ostertagi infection on secretion of metabolic hormones in calves. 146 95

Studies were performed in patients with and without renal failure to investigate the role of bacterial ammonia production in the pathogenesis of the mucosal abnormalities caused by Helicobacter pylori. The high rate of H pylori ammonia production in uraemic patients should accentuate any ammonia induced effects. The median (range) gastric juice ammonium concentration in the H pylori positive patients with renal failure was 19 mmol/l (II-43) compared with 5 mmol/l (1-11) in the H pylori positive patients without renal failure (p < 0.005). In the H pylori negative patients the values were 3 mmol/l (0.5-11) and 0.7 mmol/l (0.1-1.4) respectively in the patients with and without renal failure (p < 0.01). Despite the much higher ammonia production in the H pylori positive uraemic patients, the nature and severity of their gastritis was the same as that in the H pylori positive non-uraemic patients. The median (range) fasting serum gastrin concentration was raised in the uraemic patients compared with the non-uraemic patients but was similar in the uraemic patients with (95 pmol/l (52-333)) or without (114 pmol/l (47-533)) H pylori infection. The median (range) serum pepsinogen I concentration was also high in the uraemic compared with the non-uraemic patients and was significantly higher in uraemic patients with H pylori (352 ng/ml, range 280-653) than in those without H pylori infection (165 ng/ml, range 86-337) (p < 0.01). These findings indicate that the gastritis and hypergastrinaemia associated with H pylori infection are not the result of mucosal damage induced by the organism's ammonia production.
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PMID:Role of ammonia in the pathogenesis of the gastritis, hypergastrinaemia, and hyperpepsinogenaemia I caused by Helicobacter pylori infection. 148 61

The rise in serum gastrin and pepsinogen I after 5 days' treatment with the proton pump inhibitor pantoprazole (40 mg/day) was examined in eight duodenal ulcer patients with Helicobacter pylori infection and compared with eight in whom it had been eradicated. Before treatment, the post-prandial serum gastrin concentrations were higher in the H. pylori-positive than -eradicated patients (p less than 0.05). The median rise in pre-prandial serum gastrin concentrations on treatment was similar in the H. pylori-positive (41%) and -eradicated patients (45%). The rise in post-prandial serum gastrin was also similar in the H. pylori-positive (81%) and -eradicated patients (69%), resulting in significantly higher gastrin concentrations during treatment in the former. The median rise in serum pepsinogen I on treatment was greater in the H. pylori-positive (114%) than in the -eradicated patients (8%), resulting in significantly higher concentrations during treatment in the former. These observations indicate that eradication of H. pylori may be a means of moderating the hypergastrinaemia caused by acid-inhibitory therapy. They also indicate that H. pylori-related hypergastrinaemia is not due to an increase of the antral surface pH by the bacterium's urease activity.
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PMID:Helicobacter pylori and hypergastrinaemia during proton pump inhibitor therapy. 153 64

We evaluated the affinity of cholecystokinin octapeptide (CCK-8), gastrin, and subtype-selective CCK agonists for CCK/gastrin receptors and compared it with the ability of these peptides to stimulate phosphoinositide (PI) hydrolysis and pepsinogen release in guinea pig gastric glands. Competitive binding studies using 125I-labeled Bolton-Hunter-CCK-8 and 125I-gastrin showed the presence of CCK-B/gastrin receptors in gastric glands and dispersed chief cells. In contrast, the potency of peptides in stimulating PI hydrolysis in both gastric glands and dispersed chief cells displayed a profile similar to CCK-A receptors found in pancreatic acini, i.e., CCK-8 = A 71378 greater than A 71623 greater than A 70874 much greater than A 72962 = CCK-8 (desulfated) greater than gastrin II greater than gastrin I. In general, the rank order of potency of peptides for stimulation of PI hydrolysis correlated well with their ability to stimulate pepsinogen release. At concentrations greater than 10 microM, efficacies of gastrin I and II in stimulating pepsinogen release from gastric glands were near 90% of the maximal activity of CCK-8. The inhibitory potency of MK-329, a selective CCK-A receptor antagonist, was similar against either CCK-8 (10 nM) or gastrin I (10 microM), except that a minor portion (approximately 30-40%) of gastrin I-induced pepsinogen release was insensitive to MK-329. The MK-329-insensitive component was inhibited by CI-988, a potent and selective CCK-B/gastrin receptor antagonist.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Both CCK-A and CCK-B/gastrin receptors mediate pepsinogen release in guinea pig gastric glands. 161 41

Serum concentrations of group I pepsinogens (pepsinogen-I) and gastrin were determined in patients with dementia disorders in order to assess the relationship, if any, between these indices of gastric mucosal function and serum cobalamin (vitamin B12) levels. A significant positive correlation between pepsinogen-I and B12 and, as expected, an inverse relationship between gastrin and pepsinogen-I concentrations was found, indicating that vitamin B12 deficiency was mainly determined by gastric mucosal atrophy (atrophic gastritis) in this West-Swedish sample of patients with dementia disorders. Patients with low B12 but normal gastrin and pepsinogen-I concentrations should, therefore, be further evaluated for possible nutritional deficiency, as well as nongastric causes of poor B12 assimilation from the diet.
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PMID:Dementia patients with low serum cobalamin concentration: relationship to atrophic gastritis. 162 75

Gastrin values were evaluated in 130 parasite naive calves, in 61 first season grazing calves during six field trials and in 8 experimentally infected adult immune cows. The gastrin values were linked to pepsinogen levels and daily weight gain. Also the influence of an anthelmintic treatment on pepsinogen and gastrin values was assessed during a clinical outbreak of ostertagiosis in a group of first season grazing calves. Mean gastrin levels in parasite naive calves were 106 pg/ml. Results show that a group mean of 400 pg/ml gastrin in first season grazing calves indicates a reduced daily weight gain but with no obvious clinical signs. During clinical outbreaks mean gastrin levels frequently reached 1,000 pg/ml with a severe weight loss and a mean pepsinogen level of 5,000 mU tyr. The serum gastrin concentration was strongly reduced 4 days post treatment. No gastrin response was noted following an Ostertagia challenge in adult immune cows. The value of gastrin as a diagnostic aid for ostertagiosis is discussed in relation to pepsinogen, the adult worm burden, larval inhibition and the technique involved in assessing gastrin.
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PMID:Diagnostic value of gastrin for clinical bovine ostertagiosis. 164 75

To evaluate whether pretreatment with prostaglandin E2 (PGE2) could desensitize pepsinogen secretion in chief cells from guinea pig, chief cells were pretreated with 10 microM PGE2 for up to 30 min. Desensitization of subsequent PGE2-stimulated secretion was maximal after 15 min, averaging only 29 +/- 9% (SE) of pepsinogen secretion in control cells stimulated with 10 microM PGE2. Desensitization was half-maximal with 30 nM PGE2. PGE2 pretreatment at 4 degrees C did not cause desensitization. In cells pretreated with 10 microM PGE2 for 15 min and then given 60 min to recover, responsiveness increased to 79 +/- 7% of that for control cells stimulated with PGE2. Thus the desensitization was reversible. Pretreatment with PGD2 and PGF2a did not alter subsequent PGE2-mediated secretion. PGE2-induced desensitization was heterologous but mediator specific because pepsinogen secretion was reduced in response to adenosine 3',5'-cyclic monophosphate (cAMP)-mediated agents (secretin and vasoactive intestinal peptide) but not Ca(2+)-mediated agents (CCK-8, gastrin, or carbachol). Pretreating chief cells with 10 microM PGE2 did not significantly alter cAMP generation in response to PGE2, secretin, or 3-isobutyl-1-methylxanthine, suggesting that desensitization was not mediated by an alteration in the receptor-coupled adenylate cyclase system. Because PGE2 pretreatment also desensitized pepsinogen secretion induced by the synthetic cAMP analogues 8-BrcAMP and 2'-O-monobutyryl-8-BrcAMP, it is likely that the ability of PGE2 to desensitize pepsinogen secretion in chief cells isolated from guinea pig is due to a mechanism distal to generation of cAMP.
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PMID:Prostaglandin E2 desensitizes cAMP-mediated pepsinogen secretion in chief cells. 165 22


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