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)

The pathogenesis of peptic ulceration cannot be explained by an abnormal capacity to secrete acid, for ulcers develop in patients who secrete acid normally. Duodenal and gastric ulcers have a common cause. The location of an ulcer in each individual is primarily determined by his capacity to secrete acid at that time. There is a difference between the mechanisms which heal an ulcer and cure a patient of his disease. Procedures that reduce an individual's capacity to secrete acid, heal an ulcer by moving the focus of the ulcerogenic forces to a more proximal site. It is necessary to remove an antral factor if in addition the patient is to be cured of his disease. It is postulated that this antral factor is the gastrin (G17) which is released in abnormal amounts into gastric juice in patients with ulcers and with gastrinomas. The abnormal amount of G17 in gastric juice may be responsible for releasing abnormal amounts of G34 into the circulation from the duodenum and from gastrinomas. The abnormal release of gastrin develops as a result of an impaired response to duodenal acidification manifest in part by an impaired release of secretin. It is postulated that the abnormal stimulation of antral gastrin release may on occasions give rise to antral G-cell hyperplasia, and that the abnormal secretion of gastrin into gastric juice may on occasions give rise to gastrinomas. These abnormalities may cause ulcers by producing an uncontrolled secretion of acid and an abnormal exposure to bile.
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PMID:Is peptic ulceration a hormonal disease? 6 15

We have localized the antigenic determinants for the main forms of gastrin (big gastrin, G34, and little gastrin, G17) in hog antral mucosa using sequence specific antibodies and an indirect immunofluorescence technique. Populations of monospecific antibodies were obtained after affinity immunoadsorption to remove populations of unwanted specificity. The specificity of the purified antisera was established by direct binding of 125I labeled peptides to antisera at the same dilutions as those used in immunocytochemistry. The results indicate that in hog antral mucosa there is a single population of cells with the antigenic determinants of the C-terminal region of G17 and G34, the N-terminal region of G17, the N-terminal region of G34, and the intact G17 molecule. In duodenum there are cells with only C-terminal reactivity; since gastrin and CCK share a common C-terminal sequence it is concluded that this cell type contains CCK-like peptides rather than gastrin.
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PMID:Cellular origins of different forms of gastrin. The specific immunocytochemical localization of related peptides. 9 69

Material with gastrin-like immunoreactivity has been extracted from micro-dissected islets and from antral mucosa of normal and genetically obese mice. The islet and antral extracts cross-reacted with antisera specific for the CO2H-terminal portion of human heptadecapeptide gastrin, but did not cross-react with antisera specific for the NH2-terminal region or with an antiserum specific for the entire, intact, molecule. With the antiserum showing highest cross- reactivity, the concentration of immunoreactive gastrin in normal islet tissue (138 pmol/g, standard human G17-I) was approximately 50% that in obese mouse islets (204 pmol/g) and 2% that in normal antral mucosa (6-1 nmol/g). Following fractionation on Sephadex G-50 the principal forms of gastrin in the islet and antral extracts had similar elution volumes to human heptadecapeptide gastrin, although other, probably smaller, forms of gastrin were also noted in the islet extracts.
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PMID:Immunochemical characterization of gastrin in pancreatic islets of normal and genetically obese mice. 32 22

An intravenous bolus of pentagastrin significantly increased the amplitude and duration of oesophageal body contractions in seven patients with diffuse oesophageal spasm (DES) when compared with five normal subjects (P greater than 0.05). In order to determine whether this stimulation also occurred at physiological gastrin concentrations, the effect of an intravenous infusion of gastrin heptadecapeptide (G17), 25 pmol/kg-h, on oesophageal contractions was studied in DES patients. G17 had no significant effect on the amplitude and duration of oesophageal contractions compared with a saline control. This dose of G17 was near the D50 for gastric acid secretion and produced a rise in serum gastrin concentration comparable with a meal. G17 infusions at doses of 100 and 200 pmol/kg-h increased the amplitude and duration of oesophageal contractions, but the corresponding serum gastrin concentrations were higher than postprandial levels. Thus, endogenous fluctuations in serum gastrin heptadecapeptide, alone, are unlikely to alter oesophageal contractions in DES patients.
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PMID:Effect of gastrin heptadecapeptide (G17) on oesophageal contractions in patients with diffuse oesophageal spasm. 49 13

In normal, duodenal ulcer, and gastric ulcer subjects the two main forms of gastrin, G17 and G34, were estimated by radioimmunoassay in fasting serum and after feeding. Two antisera were used: one showing high specificity for G17, the other specific for the common COOH-terminus of G17 and G34 and so allowing estimation of G34 by difference. Basal G17 was similar in gastric ulcer, duodenal ulcer, and normal subjects and the increases of G17 after feeding were also similar in these groups. In contrast, basal G34 was similar in normal and duodenal ulcer subjects but raised in gastric ulcer subjects. After a meal the G34 concentration in both gastric and duodenal ulcer patients was significantly higher than normal. It is concluded that the higher post-prandial gastrin responses in peptic ulcer that have been previously described are due largely to increased G34.
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PMID:Big and little gastrin responses to food in normal and ulcer subjects. 52 72

In dogs with gastric fistulae and with transposition of the portal vein and the inferior vena cava, we studied secretion of acid in response to portal or systemic venous infusion of a series of progressively longer fragments of the carboxyl terminal portion of human gastrin. Pentagastrin, G6, G7, G8, G9, G10, G13, G17, and G34 were studied. Potency by portal venous infusion relative to systemic venous infusion was used as an index of hepatic inactivation. Fragments with eight or fewer amino acid residues were more than 90% inactivated by hepatic transit. Fragments with nine or more amino acid residues were more resistant to hepatic inactivation than shorter fragments. For fragments with 7 to 17 amino acid residues, increasing the chain length was accompanied by progressive increase both in hepatic resistance to inactivation and in potency for stimulation of acid secretion, suggesting that resistance to hepatic inactivation may be a major determinant of potency.
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PMID:Hepatic inactivation of gastrins of various chain lengths in dogs. 63 85

Intracellular microelectrode technique and standard organ bath technique were used to investigate the effects of pentagastrin, G17, and G34 on the electrical and mechanical activities of canine antral circular muscle. All three molecular forms increased the amplitude and duration of the plateau of the gastric action potential and the frequency of spontaneous action potentials. They also increased the amplitude and frequency of spontaneous contractions. G17 was equal to or less potent than pentagastrin in all of its actions on this tissue. G34 had an equal or greater activity than G17. The electrical studies indicate that G17 is active in this tissue in a physiological range of concentrations. The ED50 for the effect of G17 to increase the amplitude of the plateau potential is less than that for the effect of G17 on gastric secretion, indicating that this is a physiological action of gastrin. Atropine studies indicate that only part of the in vitro inotropic action of gastrin is caused by the release of acetylcholine from nerve terminals, but that the chronotropic action is attributable to a direct effect on the smooth muscle membrane.
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PMID:Effects of pentagastrin, G17, and G34 on the electrical and mechanical activities of canine antral smooth muscle. 68 Apr 95

In an attempt to confirm the reported high incidence of raised serum gastrin levels in patients with rheumatoid arthritis (RA), gastrin concentrations were estimated in 54 patients. Only three patients (6%) had basal hypergastrinaemia. The heptadecapeptide (G17) and total carboxyl-terminal immunoreactive gastrin responses to a standard protein meal were measured by specific radioimmunoassay in these three patients and in nine normogastrinaemic RA patients displaying the same age range. The three hypergastrinaemic patients showed significantly greater and more prolonged G17 and total carboxylterminal immunoreactive gastrin responses to the meal compared with the normogastrinaemic RA patients (P less than 0.02). Two of these three patients agreed to have an acid output study (pentagastrin 6 microg/kg subcutaneously) and gastric mucosal biopsies taken for histology. Both were found to be achlorhydric and to have atrophic gastritis. This study suggests that basal hypergastrinaemia in RA patients is considerably less common than previously reported and, when present, is associated with achlorhydria. In addition, the incidence of achlorhydria in rheumatoid arthritis is similar to that found in a normal age-matched population.
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PMID:Is hypergastrinaemia associated with rheumatoid arthritis? 73 75

The forms of gastrin which have been isolated from antral mucosa or Zollinger-Ellison tumour tissue (or both) and characterized chemically are as follows: little gastrin (G17) (LG); big gastrin (G34) (BG); minigastrin (G13); the NH2-terminal 1-13 fragment of G17. All these exist as pairs of peptides which have an identical amino acid sequence and differ solely in that the single tyrosyl residue present may be sulphated. The proportions of the pairs of each peptide show species variation where isolation has been accomplished (e.g. from hog, dog, cat, cow, sheep and man in the case of LG, and hog and man for BG). All these forms of the hormone have been identified immunologically in serum; LG and BG have been identified in duodenal mucosa. Two larger forms of the hormone have been identified immunologically in serum; component I (CI) and 'big big gastrin' (BBG). Material corresponding in size to BBG and CI has been identified in extracts of antral and jejunal mucosa and Zollinger-Ellison tumour. Neither BBG nor CI has been characterized chemically to date and their physiological significance is uncertain. Recent studies suggest that the heterogeneity of gastrins in serum and tissues may be considerably greater than is indicated by the list of components given above.
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PMID:Heterogeneity of the gastrins in blood and tissue. 78 76

Gastrin is a peptide hormone originating from G-cells of the antrum, the duodenum and the proximal jejunum. From extracts of gastrinomas and from sera of hypergastrinaemic subjects several gastrin molecules could be isolated which were nominated as "mini gastrin" (G13), "little gastrin" (G17), "big gastrin" (G34) and "big big gastrin". Antisera used for radioimmunological gastrin determinations should be characterized with respect to their specificity, as differeing affinity towards the various gastrins and towards CCK-PZ influences the results of the assay and thus the comparability with values of other laboratories. Gastrin is released by direct vagal stimulation of the antral G-cells and by local chemical and physical stimuli in the antrum and duodenum; probably an oxynto-pyloric reflex also exists. Gastrin stimulates in physiologic doses gastric acid secretion and, as shown in dogs and cats, reveals a trophic action on parietal cell growth. H+-secretion and gastrin release are connected by a feed back mechanism, insofar, as a decrease of intragastric pH below 3 inhibits endogenous gastrin release. Hypergastrinaemia has been demonstrated in patients with gastric anacidity or hypo-secretion, benigne pyloric stenosis, uraemia, short bowel-syndrome, gastric and duodenal ulceration and in patients with gastrinomas (Zollinger-Ellison-syndrome). Hypergastrinaemia in combination with hypersecretion exhibits clinical significance in patients suffering from Zollinger-Ellison-syndrome or excluded antrum syndrome which are due to autonomous gastrin release. The differential diagnosis between these syndromes and other diseases, in which hypergastrinaemia is not associated with gastric hypersecretion, can be achieved by several tests using calcium infusion or intravenous application of secretin and glucagon. The significance of elevated gastrin levels in patients with duodenal ulceration (DU) is pointed out. In DU-patients basal and postprandial hypergastrinaemia has been observed. In these patients gastrin release from gastric and extragastric sites is increased. In these patients hypergastrinaemia due to extragastric gastrin release could cause gastric hypersecretion at a time, when the stomach already has emptied. Furthermore parietal cell hyperplasia could be the result of chronic hypergastrinaemia.
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PMID:[Gastrointestinal hormones. I. Hormones of the gastrin group]. 87 Oct 64


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