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 a specific deoxyoligonucleotide probe to detect gastrin mRNA in poly(A)-enriched RNA preparations from hog antrum. The nucleotide sequence of the oligonucleotide, d(C-T-C-C-T-C-C-A-T-C-C-A), was deduced from the unique amino acid sequence Trp-Met-Glu-Glu of gastrin. When used with hog antral RNA, the dodecanucleotide is an effective primer for the synthesis of gastrin-specific cDNA as judged by nucleotide sequence analysis of cDNA isolated by polyacrylamide gel electrophoresis. We have determined an 81-nucleotide sequence corresponding to the region of the gastrin mRNA that codes for the known amino acid sequence of the G34 progastrin intermediate species, and we have demonstrated the presence of two consecutive basic residues preceding the G34 sequence in the prohormone. Hybridization of gastrin cDNA or synthetic dodecanucleotide to hog antral RNA separated by gel electrophoresis on agarose gels in the presence of methylmercuric hydroxide indicates that the mRNA coding for gastrin is about 620 nucleotides long. These results suggest that the gastrin precursor peptide contains 110-140 amino acids. This method should be of general application for detection and characterization of mRNAs corresponding to proteins of known amino acid sequence.
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PMID:Detection and partial sequence analysis of gastrin mRNA by using an oligodeoxynucleotide probe. 8 48

The effect of Mucaine and Aludrox on basal and food stimulated immunoreactive gastrin has been assessed in normal control subjects and patients with duodenal or gastric ulcer. No differences in gastrin responses were observed either in the basal period or after the protein meal with the two antacids. As previously described, release of gastrin was greatest in gastric ulcer patients but in contrast to previous results,normal subjects seemed to show a greater response than duodenal ulcer patients but this was not statistically significant. Thus the combination of a local anaesthetic oxethazaine with aluminium hydroxide gel does not lead to diminished gastrin release and is not the prime mechanism of action of this agent.
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PMID:The effect of mucaine on gastrin release in man. 28 54

Twelve patients with duodenal ulcers were each given on separate days and in random order an oral local anaesthetic (oxethazaine), an alkali (aluminium hydroxide and magnesium hydroxide), a combination of local anaesthetic and alkali (Mucaine), and a similar volume of water (control) followed one hour later by a solution of meat extract (Oxo). The effect of these treatments on serum gastrin levels was measured. None of the treatments altered the normal basal gastrin levels. The gastrin response to ingestion of protein extract was significantly lower in patients who had been pre-treated with local anaesthetic than those who had received alkali, with or without local anaesthetic, or water.
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PMID:The effect of oral local anaesthetic and alkali on basal and food-stimulated serum gastrin levels in patients with duodenal ulcer. 58 28

Suspension of magnesium and aluminum hydroxide (30--60 mEq/24h) or a comparable volme of water was orally administered by gastric intubation to two groups of 20 male Wistar rats each over 60 days. The antacid treatment led to a significant increase in the height (0.464 +/- 0.02 mm v. 0.318 +/- 0.06) and in the volume (472 +/- 32 mm3v.328 +/- 45) of the fundic mucosa of the stomach, in the average count of parietal cells per unit area of the mucosa (32.37 +/- 1.8 v. 22.3 +/- 1.6), and in the total parietal cell population of the stomach (53.6 +/- 3.5 x 10(6) v. 43.2 +/- 3.7 x 10(6)). Furthermore fasting serum gastrin concentration was significantly higher in the antacid treated rats (81.2 +/- 7.4 pg/ml) than in control animals (56.9 +/- 6.9 pg/ml).
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PMID:Parietal cell hyperplasia induced by long-term administration of antacids to rats. 71 Sep 69

Oral calcium carbonate (0-5 g, pH 9-4) increased serum gastrin and gastric acid output with slight but insignificant change in serum calcium. A similar rise in serum calcium during an intravenous infusion of calcium gluconate failed to increase serum gastrin and gastric acid output. Both intragastric calcium actions were abolished by acidification of the calcium carbonate solution (pH 1-0). The increase in serum gastrin and gastric acid output after intragastric calcium carbonate was not affected, however, by a simultaneous intraduodenal acid load. Equivalent neutralising doses of magnesium hydroxide (pH 9-4) did not increase serum gastrin and gastric acid output above basal levels, whereas antral acidification with 20 ml 0-1 N HCl resulted in a slight decrease in serum gastrin. Intraduodenal calcium carbonate (pH 3-0) also increased serum gastrin and gastric acid output, whereas an equivalent volume of intraduodenal saline (pH 3-0) had no effect. These findings indicate that calcium increases serum gastrin by local stimulation of antral and duodenal mucosa. They also suggest that the action of calcium on gastric secretion is partly mediated by gastrin.
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PMID:Calcium stimulation of gastrin and gastric acid secretion: effect of small doses of calcium carbonate. 87 25

The (2RS)-1,2-dipalmitoyl-3-mercaptoglycerol/-, (2RS)-1,2-dimyristoyl-3-mercaptoglycerol/-, and (2RS)-1-myristoyl-2-palmitoyl-3-mercaptoglycerol/maleoyl-bet a-alanyl- [Nle15]-human-gastrin-(2-17) adducts were prepared as lipo-gastrin derivatives of explicitly primary amphiphilic properties. As representative of this class of lipo-gastrins, the dimyristoyl derivative has been thoroughly characterized in its aggregational state since, among the three compounds, theoretically it should exhibit the lowest degree of lipid character. It aggregates in aqueous solution to form monodispersed unilamellar spherical vesicles with dislocation of the peptide moiety at the bilayer surface in predominantly unordered structure. The liposomes are remarkably stable toward solubilization with trifluoroethanol and toward vesicle to micelle transition with neutral and negatively charged surfactants even above their critical micellar concentrations. Asymmetric fusion with the detergent micelles induces polydispersion of the liposomes in terms of shape and size without affecting in significant manner the mode of display of the gastrin portions at the bilayer surface. Only the positively charged hexadecyltrimethylammonium hydroxide provokes the collapse of the vesicles into mixed micelles with concomitant altered dislocation of the gastrin-peptide in the new aggregational state. Despite the lipid properties of the gastrin derivatives, i.e., formation of liposomes, they retain remarkable receptor affinities (IC50 = 1.5 x 10(-9) M for myristoyl-palmitoyl-gastrin, IC50 = 2.0 x 10(-9) M for di-myristoyl-gastrin and IC50 = 3.1 x 10(-9) M for di-palmitoyl-gastrin vs IC50 = 2.8 x 10(-10) M for Nle15-gastrin). Since the displacement of radiolabeled Nle15-gastrin from rat pancreatic acinar cell line membrane preparations by both the parent gastrin hormone and the three lipo-gastrins occurs in parallel manner, the data support a mechanism of receptor occupancy via accumulation of the gastrins at the membrane surface and their two-dimensional diffusion to the target receptor. Thereby the differentiated decrease of affinity in function of fatty acid chain length has to be attributed to the energetically more or less favored transfer of the monomers from the donor vesicles to the acceptor membranes. Moreover, according to this model migration of the lipo-gastrins with their interdigitating di-fatty-acyl moieties should be delayed, again in lipid structure-dependent manner, in comparison to the parent gastrin molecule, which is free to float in the membrane interfacial phase.
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PMID:Peptide hormone-membrane interactions: the aggregational and conformational state of lipo-gastrin derivatives and their receptor binding affinity. 145 31

We review acid rebound, the seemingly paradoxical increase in acid secretion resulting from administration of an antacid. Primarily a laboratory observation, the demonstration of the phenomenon was a major contributing factor to the swift, and possibly unjustified, fall from grace of calcium carbonate in the therapy of peptic ulcer disease despite years of apparently successful use. Calcium, as carbonate or other salts, causes an increase in gastric acid secretion owing, at least in part, to direct ionic stimulation. Another possible mode of action involves antral alkalinization with subsequent gastrin release. Other antacids, notably magnesium hydroxide and aluminum hydroxide, may therefore also cause rebound, but the data in this area are less convincing. Despite the demonstration that acid rebound occurs, no one has thoroughly investigated its clinical import. What limited data actually exist suggest no obvious clinically significant deleterious effect from use of calcium carbonate in peptic ulcer. Because of calcium carbonate's excellent acid-neutralizing capacity, its venerable past record in treating ulcer disease, and recent observations that low-dose antacids heal peptic ulcers, it is appropriate to reevaluate acid rebound, to focus on its clinical significance, if any.
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PMID:Calcium and acid rebound: a reappraisal. 150 Jun 60

To clarify the lower esophageal sphincter (LES) pressure response to alkali ingestion, normal subjects and postantrectomy patients with either a gastroduodenostomy or gastrojejunostomy were studied in a double-blind controlled fashion. LES pressure and serum gastrin concentrations were measured after ingestion of a 100 ml bolus of either 0.4 M NaHCO3 or 0.4 M NaCl. In addition, the effect of a therapeutic dose (30 ml) of a commercial antacid preparation was studied in a double-blind fashion in 14 patients with gastroesophageal reflux disease. Peak increases in LES pressure above basal were significantly higher (p less than 0.05) after NaHCO3 than after NaCl in normal subjects and in patients with vagotomy and Billroth I antrectomy, but not in patients with vagotomy and Billroth II antrectomy. Serum gastrin concentrations were unaffected by alkali. Thirty milliliters of liquid antacid containing aluminum and magnesium hydroxide resulted in a small sustained rise in LES pressure over the first 50 min after ingestion, but this was not statistically different than the placebo response. It is suggested that: 1) neither the antrum nor intact vagi nor gastrin were required for NaHCO3 ingestion to increase LES pressure; 2) the increase in LES pressure with NaHCO3 ingestion appears to rely upon an intact duodenum and may relate to volume and osmolarity of the alkali load; and 3) therapeutic doses of a liquid commercial antacid does not significantly increase LES pressure in the presence of an intact stomach.
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PMID:Studies on the mechanism of the lower esophageal sphincter pressure response to alkali ingestion in humans. 299 Jan 96

The effects on fasting serum gastrin concentrations of hourly doses of magnesium and aluminum hydroxide antacid, with and without intravenous cimetidine, were determined in 8 patients with duodenal ulcer disease. Gastrin levels rose significantly over 10 h when antacid was given either as a bolus of 30 ml every hour or as a constant infusion of 0.5 ml/min (36 +/- 5 pg/ml and 33 +/- 6 pg/ml to 108 +/- 32 pg/ml and 109 +/- 22 pg/ml, respectively, p less than 0.05). This effect was specific for some component of the antacid and not for neutralization of acid per se, inasmuch as sodium bicarbonate, infused to keep gastric pH at levels at or above those of antacid, produced no significant rise in serum gastrin concentration. When intravenous cimetidine was administered simultaneously with intragastric antacid, gastrin levels did not rise. This occurred even though intragastric pH levels were actually higher with cimetidine plus antacid than with antacid alone. The ability of intravenous cimetidine to block antacid-induced hypergastrinemia was counteracted by infusing simultaneously both hydrochloric acid and antacid into the stomach. Since hydrochloric acid reacts with magnesium and aluminum hydroxide to form ionic magnesium and aluminum chloride, cimetidine most likely blocks antacid-induced hypergastrinemia by reducing acid secretion from the stomach and thereby limiting the generation of ionic magnesium and aluminum.
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PMID:Cimetidine blocks antacid-induced hypergastrinemia. 394 Feb 54

Antacids are neutralizing compounds which have been shown to hasten ulcer healing and to prevent bleeding from stress ulcerations. Owing to gastric alkalinization, gastrin will be released following antacid ingestion, a condition similar to that following the ingestion of a meal. Gastrin release and, more important, acid rebound also occur when the gastric mucosa comes into contact with calcium chloride. These findings indicate that acid rebound is independent of antral neutralization. Acid rebound and gastrin release will also be induced in duodenal ulcer patients by magnesium hydroxide. The magnitude of acid rebound represents one fourth to one third of the peak acid response to pentagastrin and is more marked following calcium than magnesium antacid intake. The mechanism of acid rebound may be in part due to gastrin release, but may also be due to the direct effect of calcium on the parietal cell. In the duodenum, calcium and magnesium evoke pancreatic enzyme secretion and gall bladder emptying. This effect of both cations is attributed to the release of cholecystokinin. Owing to their chemical composition, antacids stimulate the release of gastrointestinal hormones, cause acid secretion and stimulate pancreatic enzyme secretion and gall bladder concentration. So far, it has not been proven that these effects of antacids and of their chemical constituents will limit their therapeutic use.
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PMID:Antacids and hormones. 675 53


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