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)

Fortyseven uremic patients on RDT underwent a gastric secretion study and a contemporary evaluation of serum levels of Calcium (Ca), Phosphate (iP), Magnesium (Mg), Alkaline Phosphatase (AP), immunoreactive gastrin (Gas), parathyroid hormone (PTH), calcitonin (CT). Secretory test (pentagastrin 6 microgram/kg) was performed in the morning, after 12 hours of fasting, in the interdialytic interval. Female patients, male patients on RDT from less 1 year and hyposecretor patients were excluded from the study. On the basis of these criteria 25 normal or hypersecretor males between 20 and 55 years old were selected. A significant positive correlation was found between PTH and CT, while a negative significant correlation was found between CT and BAO and CT and PAO. Similarly, a significant negative correlation was found between PTH and BAO and PTH and PAO. Multiple regression study showed that the negative influence of CT on BAO and PAO is more relevant than the positive influence of PTH. These data suggest that PTH and CT are involved in gastric acid secretion in uremia. Since the inhibitory effect of CT is prevailing on the stimulating effect of PTH, patients with higher levels of PTH and CT have a lower gastric acid secretion. CT might therefore be considered as a protective factor against hypersecretion in uremia.
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PMID:Gastric acid secretion, calcitonin and secondary hyperparathyroidism in uremic patients undergoing regular dialysis therapy (RDT). 73 94

A dose response study of the effect on gastric acid secretion of synthetic human gastrin-17 (SHG) in doses of 50, 200, and 500 ng/kg/hr was performed in 8 healthy volunteers. The study was repeated on separate days during i.v. infusion of magnesium sulphate (0.4 meq Mg2+/kg/hr), of calcium gluconate (0.1 meq Ca2+/kg/hr) and of magnesium sulphate plus calcium gluconate. Magnesium infusion resulted in an increase in the dose of SHG required for one-half maximal secretion (D50), whereas infusion of calcium decreased D50. The difference in D50 of SHG when administered in combination with magnesium and with calcium was significant. Combined infusion of SHG, magnesium, and calcium resulted in the same D50 of SHG as found when SHG was infused alone. The calculated maximal acid response was almost identical in the four experiments except for a minor but nonsignificant decrease during calcium infusion. The results indicate an interaction of calcium, magnesium, and gastrin on parietal cell function and extend the observations of others in intact humans as well as in isolated gastric mucosa.
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PMID:Interaction of calcium, magnesium, and gastrin on gastric acid secretion. 75 48

Binding of 125I-[Nle15]gastrin to albumin purified from porcine serum, from porcine gastric mucosal cytosol, and from bovine serum has been demonstrated by covalent cross-linking and ultracentrifugation. Binding was enhanced in the presence of Zn2+, Ni2+, Cu2+, Co2+, and Cd2+, but not Ca2+, Mg2+, or Mn2+. The best fit to the binding data for bovine serum albumin was obtained with a model assuming two nonequivalent binding sites. The affinity of both sites for gastrin was increased in the presence of 100 microM Zn2+ or Ni2+ ions. The highest association constant observed was 2.3 X 10(5) M-1 in the presence of 100 microM Zn2+ ions. The similarity of the Zn(2+)-dependence of binding for bovine and porcine serum albumins, despite the replacement of His3 by Tyr, suggested that the N-terminal metal ion-binding site was not involved. Although all gastrin affinities were reduced by 50% in the presence of 150 mM NaCl, the Zn(2+)-dependence of binding was retained. We therefore propose that the ternary complex of gastrin, Zn2+ ions, and albumin may play a physiological role in the serum transport of Zn2+ ions and in the uptake of Zn2+ ions from the lumen of the gastrointestinal tract.
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PMID:Metal ion-dependent binding of gastrin to albumin. 195 45

The binding of cholecystokinin (CCK) to its receptors on guinea pig gastric chief cell membranes were characterized by the use of 125I-CCK-octapeptide (CCK8). At 30 degrees C optimal binding was obtained at acidic pH in the presence of Mg2+, while Na+ reduced the binding. In contrast to reports on pancreatic and brain CCK receptors, scatchard analysis of CCK binding to chief cell membranes revealed two classes of binding sites. Whereas, in the presence of a non-hydrolyzable GTP analog, GTP gamma S, only a low affinity site of CCK binding was observed. Chief cell receptors recognized CCK analogs, with an order of potency of: CCK8 greater than gastrin-I greater than CCK4. Although all CCK receptor antagonists tested (dibutyryl cyclic GMP, L-364718 and CR1409) inhibited labeled CCK binding to chief cell membranes, the relative potencies of these antagonists in terms of inhibiting labeled CCK binding were different from those observed in either pancreatic membranes or brain membranes. The results indicate, therefore, that on gastric chief cell membranes there exist specific CCK receptors, which are coupled to G protein. Furthermore, chief cell CCK receptors may be distinct from pancreatic or brain type CCK receptors.
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PMID:Characterization of cholecystokinin receptors on guinea pig gastric chief cell membranes. 199 75

Specific binding sites for human gastrin I (gastrin) were identified in a crude membrane preparation from the gastric carcinoid tumor of Mastomys (Praomys) natalensis. The binding of 125I-gastrin to the carcinoid tumor membrane was saturable, and Scatchard analysis of the data revealed a single class of binding site with a dissociation constant of 139.2 pM and a maximal binding capacity of 23.5 fmol/mg protein. Gastrin and CCK8 equipotently and dose-dependently displaced the binding of 125I-gastrin to the membrane. GTP but not ATP decreased 125I-gastrin binding to the membrane, and removal of Mg2+ attenuated this inhibitory action of GTP. The GTP-induced reduction of 125I-gastrin binding was found to be due to a decrease in binding affinity without a change in binding capacity. These results clearly indicate the presence of specific binding sites for gastrin, probably coupled to guanine nucleotide-binding protein, in the carcinoid tumor membrane of Mastomys, and suggest that gastrin has possible biological actions on these tumors.
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PMID:Receptors for gastrin on gastric carcinoid tumor membrane of Mastomys natalensis. 204 96

Cholecystokinin (CCK) binding sites were solubilized from pig cerebral cortical membranes with digitonin (2%, w/v) in the presence of Na+ (120 mM) and Mg2+ (5 mM). Scatchard plot transformation of equilibrium binding data obtained with 125I-CCK-8S gave an apparent dissociation constant (Kd) of 0.6 nM, comparable to that obtained in membranes in the presence of these cations. Hill coefficients close to unity suggested the presence of a single population of receptor sites. Competitive inhibition studies with pentagastrin, gastrin(1-17)S and the CCKA receptor antagonist L-364,718 indicated that the solubilized receptor sites were of the B-type (CCKB), with the same pharmacological profile as that observed in membranes. Optimal specific binding of 125I-CCK-8S to membrane-bound and solubilized receptors was obtained in the presence of divalent cations. Both the membrane-bound and the solubilized receptor activity were attenuated by guanylyl-imidodiphosphate (Gpp(NH)p) indicating that the brain CCKB receptors are coupled to G proteins.
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PMID:Solubilization and characterisation of the cholecystokininB binding site from pig cerebral cortex. 258 45

The accessibility of nucleotides in Escherichia coli tRNAfMet to chemical and enzymatic probes in the presence and absence of methionyl-tRNA synthetase has been investigated. Dimethyl sulfate was used to probe the reactivity of cytosine and guanosine residues. The N-3 position of the wobble anticodon base, C34, was strongly protected from methylation in the tRNA-synthetase complex. A synthetase-induced conformational change in the anticodon loop was suggested by the enhanced reactivity of C32 in the presence of enzyme. Cytosine residues in the dihydrouridine loop and in the 3'-terminal CCA sequence showed little or no change in reactivity. Methylation of the N-7 position of guanosine residues G42, G52, and G70 was partially inhibited by the synthetase. Nuclease digestion of tRNAfMet with alpha-sarcin in the presence of 1-2 mM Mg2+ resulted in cleavage mainly at C71 in the acceptor stem and was strongly inhibited by synthetase. Other nuclease digestion experiments using the single strand specific nucleases RNase A and RNase T1 revealed weak protection of nucleotides in the D loop and strong protection of nucleotides in the anticodon on complex formation. The present data, together with previous structure-function studies on this system, indicate strong binding of methionyl-tRNA synthetase to the anticodon of tRNAfMet, leading to a change in the conformation of the anticodon loop and stem. We propose that this, in turn, produces more distant, and possibly relatively subtle, conformational changes in other parts of the tRNA structure that ultimately lead to proper orientation of the 3' terminus of the tRNA with respect to the active site of the enzyme.
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PMID:Study of the interaction of Escherichia coli methionyl-tRNA synthetase with tRNAfMet using chemical and enzymatic probes. 309 57

The purpose of this study was to examine the effect of three common divalent cations (Ca2+, Mg2+, and Zn2+) on the release of cholecystokinin (CCK-33), pancreatic polypeptide (PP), and gastrin. Five dogs with pancreatic and gastric fistulas were given 1-h intraduodenal infusions of calcium (5 mmol X kg-1 X h-1), magnesium (4 mmol X kg-1 X h-1), or zinc (1 mmol X kg-1h-1). At another time the same dogs were given an intravenous bolus followed immediately by a 1-h infusion of calcium (0.36 mmol/kg [bolus], 0.36 mmol X kg-1 X h-1), magnesium (0.25 mmol/kg [bolus], 0.25 mmol X kg-1 X h-1), or zinc (0.03 mmol/kg [bolus], 0.03 mmol X kg-1 X h-1). Intraduodenal infusions of calcium, magnesium, and zinc significantly stimulated CCK-33, PP, and gastrin release. Intravenous calcium stimulated CCK-33, PP, and gastrin release to 245, 193, and 155% of basal levels, respectively. Intravenous magnesium increased CCK-33 to 123% of basal levels but did not stimulate PP and gastrin levels. Intravenous zinc stimulated release of CCK-33, PP, and gastrin to 126, 185, and 124%, respectively. This study shows that calcium, magnesium, and zinc can stimulate release of CCK-33, PP, and gastrin in much the same manner. We suggest that these cations may have a nonspecific electrical action that results in an alteration of membrane permeability, which leads to release of gastrointestinal hormones.
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PMID:Effect of divalent cations on gastrointestinal hormone release and exocrine pancreatic secretion in dogs. 396 59

The effect of the C-terminal octapeptide of cholecystokinin-pancreozymin (CCK-PZ), caerulein, and the C-terminal tetrapeptide of gastrin on pancreatic secretion of fluid, electrolyte, amylase, and protein was studied in anaesthetized dogs prepared with pancreatic fistulae. Against background stimulation of fluid secretion with submaximal doses of secretin, all the polypeptides produced a qualitatively similar pancreatic response, causing a highly significant increase in amylase, protein, calcium, and zinc concentrations. Magnesium concentration was significantly increased only when the concentration preceding the administration of the peptide was below 100 mu-equiv/l. Octa-CCK-PZ was 13-35 times and 20-56 times more potent than tetragastrin on weight and molar bases, respectively, as a stimulant of amylase secretion. The threshold doses were largest for amylase, lower for calcium, and lowest for zinc. A significant linear correlation was observed between amylase and calcium concentration, zinc and protein concentration, and magnesium and calcium concentration. The peptides produced some increase in secretin-induced volume flow, whereas bicarbonate, chloride, sodium, and potassium concentrations remained unchanged. The direct relation between bicarbonate concentration and flow rate was limited to rates below 1.5 ml/5 minutes. At higher rates bicarbonate and chloride concentration reached a high and low plateau, respectively, although the first five-min sample of pancreatic juice after secretin stimulation exhibited a relatively low bicarbonate and high chloride concentration compared with its voluminous flow. Chloride concentration varied inversely with bicarbonate concentration, the sum of the two anions being constant.
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PMID:The action of the C-terminal octapeptide of cholecystokinin and related peptides on pancreatic exocrine secretion. 474 91

1 A rat isolated gastric mucosal preparation was used to monitor histamine output and acid secretion during stimulation by different secretagogues. 2 In non-stimulated preparations, spontaneous histamine output decreased over 450 min. 3 Stimulation of secretion with 4 (5)-methylhistamine or dibutyryl cyclic adenosine 3'5'-monophosphate (db cyclic AMP) and theophylline did not influence histamine output. 4 Pentagastrin, gastrin and methacholine increased both acid secretion and histamine output. Pentagastrin and gastrin mobilized six times more histamine and relation to acid secretion than did methacholine. 5 Spontaneous histamine output and secretagogue-induced increases were unaffected by changes in external Ca2+ (0.0 to 7.2 mM) or Mg2+ (1.2 to 4.8 mM). 6 These results support the hypothesis that mucosal histamine plays a more important role in the action of gastrin than of cholinomimetics on the parietal cell.
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PMID:Increased histamine-output from the isolated gastric mucosa of the rat in response to pentagastrin and methacholine. 617 70


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