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)

A women had hypergastrinaemia associated with the variety of gastritis (Type A) that is associated usually with pernicious anaemia, together with recurring bouts of severe abdominal pain. Fasting serum gastrin levels ranged between 600 and 2750 pg/ml. There was a rise in serum gastrin levels after a standard protein meal, indicative of a large G cell mass, and a fall after intragastric HCI, which led to a trial of treatment with HCI; this gave some symptomatic relief. After surgical antrectomy there was a profound fall of serum gastrin from a pre-operative level of 2500 pg/ml to constant values of 16--25 pg/ml, and complete and lasting relief from the bouts of abdominal pain.
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PMID:Symptomatic hypergastrinaemia with achlorhydria: reflief by antrectomy. 105 75

Gastrin is released by food rich in proteins and by vagal mechanisms. HCI and possibly secretin and glucagon inhibit gastrin release. In the wide range of actions of gastrin, stimulation of gastric acid secretion is the most important. With the advent of radioimmunochemical methods for the determination of gastrinaemia, it has been shown that gastrin exists in a number of forms of different molecular weight. To estimate the validity of gastrin radioimmunoassay it is necessary to demonstrate that decrease in antibody-bound labelled antigen is unrelated to non-specific interference by unknown substances present in serum samples, and that the antiserum reacts with endogenous hormone in an identical manner. Heterogeneity of gastrin in serum may affect the validity of the radioimmunoassay. Hypergastrinaemia associated with hyper-normochlorhydria occures in gastrinoma, hyperplasia of antral gastrin cells, diseases with delayed gastric emptying, retained antrum, short bowel syndrome,renal failure. Hypergastrinaemia associated with hypo-achlorhydria occurs in atrophic gastritis without extensive antral lesion and after vagotomy. Gastrin radioimmunoassay can be used for the mass screening of subjects with atrophic gastritis, a high risk group for gastric cancer.
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PMID:[Gastrin]. 123 74

H,K-ATPase from gastric mucosa is responsible for HCI secretion in the gastric lumen and is a member of the P-type ATPase family. The structure of enzyme subunits, their functions and topology, the mechanism of ATP hydrolysis and transport function of the enzyme, its specific inhibitors, and the success of their pharmacological application are reviewed. The methods for isolation of membrane fractions with H,K-ATPase activity and attempts for solubilization and purification of the enzyme are described. Data demonstrating the presence of H,K-ATPase in other tissues are considered. Information about other enzyme systems of parietal cells involved in transepithelial transport of HCl (the Cl- and K-channels of the apical membrane, the HCO3-/Cl- anion exchanger and Na+/H+ cation exchanger of the basolateral membrane) is presented. Mechanisms of activation of acid secretion by parietal cells via gastrin, acetylcholine, and histamine receptors and the role of cytoskeletal proteins in activation are reviewed.
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PMID:H,K-ATPase and acid secretion control in gastric mucosa. 946 28

The association of Helicobacter pylori with gastritis, peptic ulcers, and gastric neoplasia has led to fundamental changes in the understanding of gastric disease in humans. The relationship of Helicobacter spp. infection to gastric disease in dogs is unclear. The objective of this study was to determine if Helicobacter infection affects the gastric secretory axis of dogs. Eight Beagle dogs with naturally acquired Helicobacter spp. infection were studied before and after (4 and 29 days) the attempted eradication of Helicobacter spp. with a combination of amoxicillin, metronidazole, and famotidine (AMF). Six specific-pathogen-free, Helicobacter-free Beagle dogs served as controls. The electron microscopic appearance of spiral organisms in infected dogs indicated coinfection with Helicobacter felis- and H bizzozeronii-like organisms. Unstimulated gastric pH and fasting, postprandial, and bombesin-stimulated plasma gastrin were similar in both infected and uninfected dogs, although a trend (P = .09) toward higher meal-stimulated gastrin was observed in infected dogs at 60 minutes. Pentagastrin-stimulated maximal acid output (mmol HCI/kg0.75/hour) and titratable acidity (mmol HCl/mL) were similar in both infected and uninfected dogs, but gastric pH during maximal acid output was lower (P < .01) in uninfected dogs. Mild gastric inflammation was present in both infected and uninfected dogs. Gastric spiral organisms were undetectable in 6/8 infected dogs 4 days after AMF but had recurred in 8/8 dogs 29 days after AMF. Analysis of gastric DNA with Helicobacter-specific primers indicated persistence of Helicobacter DNA at 4 and 29 days after antibiotic therapy. Acid secretion, plasma gastrin, and mucosal inflammation were not affected by the transient suppression of Helicobacter spp. by AMF. These findings suggest that gastric secretory function in dogs is not markedly perturbed by naturally acquired Helicobacter spp. infection and that treatment with amoxicillin, metronidazole, and famotidine causes suppression rather than eradication of gastric Helicobacter spp. in dogs.
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PMID:Gastric function in dogs with naturally acquired gastric Helicobacter spp. infection. 1058 48

We describe a case of multiple gastric carcinoid tumors in a 47 year-old Japanese man. The patient had markedly elevated serum gastrin levels (>800 pg/mL), which were suppressed by secretin-pancreozymin administration. In the partial gastrectomy specimen, a total of 19 carcinoids arose from diffuse linear and micronodular hyperplasia of the oxyntic mucosal endocrine cells. The carcinoid cells were chromogranin A-positive. Except for a very small number of serotonin-positive cells in several carcinoids, none of the 19 reacted with a battery of antibodies to other bioactive neuroendocrine substances. The most prominent findings in this case were peculiar fundic glands that were distended with a proteinaceous substance and lined with large hypertrophic parietal cells. At the ultra-structural level, these cells showed poorly developed intracytoplasmic canaliculi and vesicotubular profiles, yet their large cytoplasm had numerous mitochondria. On the basis of our histological and ultrastructural findings we suggest that an intrinsic HCI secretion abnormality of the parietal cells may be responsible for the patient's hypergastranemia. Since there have been no reports on similar parietal cells changes, it is possible that our case may represent a pathological entity not previously described.
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PMID:An Unusual Case of Multiple Gastric Carcinoids Associated with Diffuse Endocrine Cell Hyperplasia and Parietal Cell Hypertrophy. 1211 44