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)

We have used immunochemical, chromatographic, and bioassay techniques to characterize peptides related to gastrin and CCK, from the stomach of the reptile Crocodylus niloticus. By immunocytochemistry gastrin/CCK-like peptides were localized in specific mucosal cells of the pylorus and in the duodenum. Boiling water extracts of pyloric antrum cross reacted with four antisera specific for the C-terminal region of gastrin or CCK, but estimates of concentration varied between antisera. Antisera specific for the N-terminus of heptadecapeptide gastrin (G17), intact G17, or the amphibian CCK-like peptide caerulein did not cross react with the crocodile extracts. Gel filtration of the extracts on Sephadex G50 resolved one major peak eluting significantly before G17 or CCK8, suggesting larger molecular size, whereas ion exchange on DE52 cellulose resolved two major immunoreactive peaks, both eluting before G17, indicating that they are less acidic. The more acidic of the two peptides stimulated gastric acid secretion in the rat, but had no CCK-like actions on the rat pancreas. Thus crocodile antrum contains gastrin-like peptides, which are however clearly distinguishable from any of the known mammalian forms of gastrin and CCK.
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PMID:Biologically active gastrin/CCK-related peptides in the stomach of a reptile, Crocodylus niloticus; identified and characterized by immunochemical methods. 716 3

We studied 25 duodenal ulcer patients and 14 age- and sex-matched normal controls to determine whether gastric acid secretion in duodenal ulcer patients is abnormally sensitive to stimulation by gastrin endogenously released in response to meals. Acid response to saline and to 0.5, 1.0, 2.0, 4.0, and 8.0% peptone infused into the stomach was measured by 30 min intragastric titration. Total serum gastrin (G-total) and serum heptadecapeptide gastrin (G17), fasting and 30 min after each test meal, were measured by specific radioimmunoassays. In 19 ulcer patients and 11 normal subjects (controls), acid response to graded doses (11, 33, 100, and 300 pmol kg(-1) h(-1)) of G17-I were also measured. Mean acid output in response to each dose of peptone was significantly higher in duodenal ulcer patients than in the controls. Gastrin levels in ulcer patients and controls were not significantly different. Within individual patients and controls, both G-total and G17 were significantly correlated with meal-stimulated acid output regardless of whether the absolute, basal-corrected, or distention-corrected values for acid output were examined (median r ranged from 0.82 to 0.94, P < 0.001). From the individual regression lines, the gastrin concentrations corresponding to half of the highest observed meal-stimulated acid response (D(50m)) were calculated. Mean D(50m) for G-total and G17 were significantly lower in duodenal ulcer patients than in controls both in the overall group and in pairs of ulcer patients and controls matched on the basis of highest observed meal-stimulated acid responses, or on the basis of maximal acid output in response to synthetic human G17. The dose of exogenously administered G17 required for half maximal G17 acid response mean D(50g), was significantly less in patients than in control subjects. In both ulcer and control subjects, D(50g) correlated significantly with D(50m). This and the significant correlation between meal-stimulated G17 and acid response strongly suggest that the endogenously released gastrin was responsible for most, if not all, of the postpeptone acid output.We conclude that after peptone test meals, gastric acid secretion in duodenal ulcer patients was abnormally sensitive to stimulation by endogenously released gastrin.
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PMID:Gastric acid secretion is abnormally sensitive to endogenous gastrin released after peptone test meals in duodenal ulcer patients. 735 94

The fine structural alteration in the gastric nerve fibers containing gastrin-releasing peptide (GRP) was studied in relation to the dynamics of gastrin-producing cells (G-cells) after truncal vagotomy in a rat model. The circulating gastrin levels were markedly elevated from the 1st day after vagotomy and the number of G-cells with positive immunoreaction for G17 and G34(1-15) was significantly increased in the vagotomized group. On the 3rd day after vagotomy, the G-cells showed conspicuous ultrastructural changes characterized by hypertrophy of the Golgi complexes and increased numbers of secretory granules. The GRP-positive nerve fibers formed a fine network in the gastric wall and were densely distributed in the oxyntic mucosa close to the blood vessels and showing varicosities composed of either small clear or GRP-positive large vesicles containing an electron-dense core. In the oxyntic mucosa of the vagotomized rats, axonal swelling of the nerves occurred on the 3rd day, and a depletion of GRP immunoreactivity was evidenced by a markedly decreased number of large-cored vesicles on the 7th day, when the serum GRP levels were also found to be markedly elevated. These findings indicate that the alteration in gastric nerve fibers containing GRP after truncal vagotomy may be related to hypergastrinemia and antral G-cell hyperplasia in the rat gastric mucosa.
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PMID:Alteration in gastric nerve fibers containing gastrin-releasing peptide in relation to the gastrin-producing cell population after truncal vagotomy in a rat model. 764 Apr 68

The precursor of the acid-stimulating hormone gastrin gives rise to multiple peptides differing markedly in biological activity, but the relevant biosynthetic pathways are poorly understood. We have used antibodies to amidated gastrins, gastrins with COOH-terminal glycine (Gly) gastrins with COOH-terminal hydroxyglycine (GlyOH) and to the COOH terminus of progastrin, to immunoprecipitate peptides labeled with [35S]sulfate or [3H]tyrosine during incubation of rat antral mucosa in vitro. Labeled progastrin was detectable after 30 min of continuous incubation with isotopic precursors, G34 and G34-Gly after 60 min, and G17 and G17-Gly after 120 min. Pulse chase experiments indicated that progastrin is converted to G34-Gly which then follows one of two pathways: (a) hydroxylation of COOH-terminal Gly and conversion to G34 followed by cleavage yielding G17, or (b) cleavage to G17-Gly. The kinetics of G17-Gly and G17 labeling were similar, suggesting that G17-Gly is a product in its own right, and not simply an intermediate in G17 synthesis. Since the two peptides are reported to have distinct biological activities, they appear to be alternative mature products of progastrin processing.
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PMID:Pathways of processing of the gastrin precursor in rat antral mucosa. 770 72

Helicobacter pylori is a microaerophilic bacterium initially found in the gastric antrum of patients with peptic ulcer disease. As a result, H. pylori is now believed to have a pathophysiologic role in gastritis as well as in peptic ulcer disease. Several recent studies showed that it may be associated with duodenal ulcer relapse and that eradication therapy using antibiotics may significantly decrease the ulcer recurrence rate in duodenal ulcer patients. Moreover, epidemiological studies suggest that it may increase the relative risk of carcinoma in the stomach and preliminary studies seem to indicate that some low-grade lymphoma in the stomach may regress after H. pylori eradication. Although the mechanisms by which H. pylori induces mucosal injury and/or neoplasm is not clearly understood, several modifications in gastric functions have been reported. The most specific way of detecting H. pylori in tissue is a combination of culture and histologic staining of mucosal biopsy specimens obtained by endoscopy. Rapid urease test, cytology and PCR procedures performed on biopsies may give rapid, sensitive and specific results. Breath test using 13C- or 14C-radiolabelled urea and serology tests are of particular importance when H. pylori diagnosis is needed via no invasive procedures. Helicobacter pylori is supposed to interact with G and D cells. Gastrin and somatostatin are synthetized and released from antral G and gastric D cells respectively. The gastric D cells are in close contact with either G and parietal cells. Gastrin stimulates gastric acid secretion and epithelial gastric cell proliferation (parietal and EC-L cells) while somatostatin inhibits these effects. Chronic gastritis is associated with fundic duodenal ulcer disease. In this situation, basal gastrin and meal- or bombesin-stimulated gastrin in the serum (especially gastrin G17) have been found to be higher in H. pylori positive than in negative patients. Moreover, gastrin decreases up to normal levels after eradication of H. pylori. The long term effect of a such hypergastrinemia is not so far established. The mechanism underlaying hormonal modification is poorly understood. Since no G/D cell ratio modification could be found after H. pylori eradication while the amount of somatostatin increases, one would suggest functional alteration of either G or D cells in the H. pylori-related chronic gastritis. The role of inflammatory mediators on the gastrin release and the processing of progastrin induced by the bacterium need further investigations.
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PMID:[Helicobacter pylori, a rediscovered bacterium. Implication in gastroduodenal diseases]. 789 50

1. In adult sheep and in lambs, over 95% of gastrin in the abomasal antrum was G17 with small amounts of G34 and lesser amounts of Component I. 2. Low gastrin concentration in the proximal duodenum was associated with a reduced percentage of G17. 3. The proportion of G34 increased progressively down the duodenum from a mean of 7% proximally to 47% in the most distal segment, and correlated negatively in any segment with the gastrin content. 4. In both the antrum and proximal duodenum, 60-70% of the G17 was in the sulphated form. 5. The gastroepiploic venous serum contained less G17 and more G34 than the tissues and up to 19% G14.
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PMID:Low tissue gastrin content in the ovine distal duodenum is associated with increased percentage of G34. 809 47

The presence and distribution of cholecystokinin (CCK)/gastrin-like immunoreactivity (IR) was examined in the goldfish pituitary. Intense CCK/gastrin-like IR was consistently observed within fibers of the proximal pars distalis (PD), with fewer IR fibers localized in the rostral PD. Within the proximal PD CCK/gastrin-like IR fibers were distributed among both the gonadotrophs and somatotrophs, suggesting a possible role for CCK-like peptides in the regulation of gonadotropin-II (GtH-II) and growth hormone (GH) secretion. Exposure of pituitary fragments from either sexually gonadal recrudescing (maturing) or regressed goldfish to three 5-min pulses of 1.0 or 10 nM sulfated CCK8 (CCK8-s), at 55-min interpulse intervals, resulted in an increased secretion of both GtH-II and GH. Independent of the dose perifused, the GtH-II release responses to the second and third pulses of CCK8-s were always of similar magnitude to the first pulse at a given dose. For GH, repeated challenges of pituitary fragments to 0.1 or 1.0 nM CCK8-s stimulated release responses of similar magnitude; however, successive pulses of 10 nM CCK8-s resulted in a desensitization in the GH release response to the second or the third pulse. Fragments from sexually regressed goldfish exhibited an overall greater release response of GtH-II to CCK8-s relative to fragments from sexually recrudescing fish, whereas the GH release responses to CCK8-s were similar between the two sexual stages. A dose-dependent release of GtH-II was present in pituitary fragments from sexually regressed goldfish following five 5-min pulses of increasing (0.1 to 100 nM) doses of CCK8-s. Finally, the sulfated forms of CCK8 and gastrin 17 (G17-s) exhibited greater stimulatory abilities than the nonsulfated form of CCK8 in releasing GtH-II and GH from fragments of sexually recrudescing fish. Additionally, CCK8-s and G17-s were equal in their capacity to stimulate the release of GtH-II, whereas G17-s was slightly more effective than CCK8-s in stimulating the release of GH. Overall, these studies are the first to provide evidence that IR CCK/gastrin-like fibers are codistributed among the gonadotrophs and somatotrophs, and that CCK-like peptides are highly effective in stimulating GtH-II and GH release from the goldfish pituitary.
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PMID:CCK/gastrin-like immunoreactivity in the goldfish pituitary: regulation of pituitary hormone secretion by CCK-like peptides in vitro. 826 60

Helicobacter pylori infection increases the serum concentration of gastrin, and this may be one of the mechanisms by which it predisposes to duodenal ulceration. Different forms of circulating gastrin were studied both basally and postprandially in 13 duodenal ulcer patients before and one month after eradication of H pylori. Three antisera that are specific for particular regions of the gastrin molecules were used. Gel chromatography indicated that > 90% of the circulating gastrin consisted of gastrin (G) 17 and G34 both before and after eradicating the infection. The basal median total immunoreactive gastrin concentration fell from 26 pmol/l (range 11-43) to 19 pmol/l (8-39) (p < 0.05), entirely because of a fall in G17 from 6 pmol/l (< 2.4-25) to < 2.4 pmol/l (< 2.4-23) (p < 0.001). The median (range) basal G34 values were similar before (15 pmol (2-36)) and after (10 pmol (2-30)) eradication. The median total immunoreactive gastrin concentration determined 20 minutes postprandially fell from 59 pmol/l (38-114) to 33 pmol/l (19-88) (p < 0.005), and again this was entirely the result of a fall in G17 from 43 pmol/l (9-95) to 17 pmol/l (< 2.4-52) (p < 0.001). The median postprandial G34 values were similar before (13 pmol/l, range 6-42) and after (15 pmol/l, range 6-30) eradication. Eating stimulated a noticeable rise in G17 but little change in G34, both in the presence and absence of H pylori. The finding that H pylori infection selectively increases G17 explains why the infection causes mainly postprandial hypergastrinaemia. G17 is increased selectively because H pylori predominantly affects the antral mucosa which is the main source of G17 whereas G34 is mainly duodenal in origin. This study also indicates that the increased concentration of gastrin in H pylori infection is the result of an increase in one of the main biologically active forms of the hormone.
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PMID:Helicobacter pylori related hypergastrinaemia is the result of a selective increase in gastrin 17. 831 7

Patients referred to us with "positive" secretin tests and the diagnosis of Zollinger-Ellison syndrome were found to be achlorhydric. This observation led us to study prospectively the accuracy and precision of serum gastrin determinations from commercial laboratories. Synthetic gastrin (G17) was added to serum to achieve gastrin concentrations of 50, 100, 250, 500, 750, 1000, 3000, and 5000 pg/mL after subtraction of the basal value (24 pg/mL). Three aliquots of each concentration were analyzed by radioimmunoassay in our laboratory (Health Science Center at Brooklyn) and sent to four major commercial laboratories that perform 5000 to 25,000 gastrin assays per year. The reported gastrin concentrations of the triplicate samples demonstrate that many commercial laboratories failed to accurately measure gastrin. Commercial laboratories generally reported higher-than-actual gastrin concentrations in samples containing less than 500 pg/mL and lower-than-actual gastrin concentrations in samples containing more than 500 pg/mL. Of all aliquots containing 100 pg/mL or less, 14 of 24 samples (58%) were reported by commercial laboratories to contain elevated gastrin concentrations. At gastrin concentrations from 250 to 5000 pg/mL, the range of values (highest- to lowest-reported value for each concentration) was greater than 200 pg/mL in 62% of triplicate samples reported by commercial laboratories. These data indicate that determinations by some commercial laboratories lack the precision required to satisfy the current diagnostic criterion (a postsecretin rise from basal gastrin of 200 pg/mL or greater) for Zollinger-Ellison syndrome. Clinicians should be aware of this problem and obtain more basal serum gastrin samples to allow for an analysis of the range of baseline values prior to secretin injection.
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PMID:Accuracy and precision of serum gastrin measurements in commercial laboratories. 852 Jan 76

It has been reported in the literature that a large quantity of gastrin is released into the gastric lumen in various species. This study was aimed to examine the stability of gastrin in the gastrointestinal (GI) lumen of pigs. Iodine-labelled little (G17) and big gastrin (G34) were incubated in vitro with the GI luminal fluids of suckling, weanling and adult pigs at 37 degrees C for 20 min, and the degradation of the peptide was measured by monitoring the generation of trichloroacetic acid soluble radioactivity. The degradation rate of G17 in the gastric fluids of all animals was less than 10%, while the degradation of G34 was less than 15% in the gastric fluids of suckling and adult pigs and about 25% in the gastric fluids of weanling pigs. The degradation rates of G17 and G34 in the small intestinal fluids of suckling pigs were between 18 and 30%, and were significantly lower than the corresponding rates in the intestinal fluids of weanling and adult pigs, the latter were between 35 and 67%. Addition of defatted porcine colostrum or its components, the casein or acid-soluble fraction, inhibited gastrin degradation in the intestinal fluids with the casein fraction having highest inhibition potency. These results indicate that gastrin is stable in the GI lumen of the suckling pigs and porcine colostrum protects gastrin from luminal hydrolysis in the small intestine, suggesting a potential physiological role of luminally released gastrin in suckling animals.
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PMID:Stability of gastrin in the gastrointestinal lumen of suckling, weanling and adult pigs. 885 48


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