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 advent of the H2-histamine-receptor antagonists has given new life to the old hypothesis that histamine might be the final common chemical mediator of acid secretion. The available evidence, however, does not prove this hypothesis but does confer on histamine a role in the regulation of acid secretion in normal physiology. Evidence is mounting that, in addition to its stimulatory action, the vagus may play an inhibitory role in acid secretion and gastrin release. Our concepts of the gastric phase of acid secretion have been extended by the discovery of cross distension reflexes in the stomach: the pyloro-oxyntic reflex for acid secretion and the oxyntopyloric reflex for gastrin release. In addition, digested protein has been shown to stimulate directly the oxyntic gland mucosa, but the evidence is against a role for this mechanism in the intact stomach. The hormone(s) responsible for the intestinal phase have not been isolated but the physiological characteristics of entero-oxyntin (a nongastrin, enteric substance that acts on the oxyntic cell) have been defined. Gastric inhibitory polypeptide is an excellent candidate for the entero-gastrone released by fat, but whether it is the sole enterogastrone released is yet to be determined.
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PMID:Regulation of gastric acid secretion. 1 82

The effects of metiamide, a histamine H2-receptor antagonist, and propranolol, a beta-adrenergic blocking agent, on gastric secretion were studied in anesthetized dogs. Metiamide, 1.45 mg/kg i.v., markedly inhibited the gastric secretion induced by a continuous i.v. infusion of tetragastrin (8 microng/kg-hr), histamine dihydrochloride (160 microng/kg-hr), or methacholine bromide (100 microng/kg-hr). Propranolol 0.5 or 1.0 mg/kg i.v. produced a significant potentiation of tetragastrin-induced gastric secretion but no influence of the secretion induced by methacholine. Propranolol at 5 or 10 mg/kg i.v. produced a slight reduction of the tetragastrin-induced secretion and a significant reduction of methacholine-induced secretion. Histamine-induced gastric secretion was not affected by propranolol at either 1 and 10 mg/kg i.v. These findings lend support to the hypothesis that interactions among histamine, gastrin and acetylcholine receptors do occur though the degree would not be the same in all directions.
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PMID:Effects of metiamide and propranolol on gastric secretion in anesthetized dogs. 1 25

Twenty-three patients with hyperparathyroidism from six families with the multiple endocrine adenomatosis (MEA) I-syndrome were tested by secretin provocation. In nine cases this led to increases in serum gastrin ranging from 298 to 13 300 pg/ml, whereas the maximum rise in gastrin in the other 14 patients was 32 pg/ml. In all nine patients with marked gastrin responses to secretin, the Zollinger-Ellison syndrome was diagnosed by gastric acid hypersecretion and large increases in gastrin after calcium administration. Six of these nine patients had, at most, minor postprandial rises in gastin and two had demonstrable tumors. In 34 normal subjects, 23 nonaffected members of families with MEA I-syndrome, and 42 patients with various diseases the maximum gastrin response to secretin was 21 pg/ml. We conclude that secretin provocation is helpful in the diagnosis of the Zollinger-Ellison syndrome, especially when basal serum gastrin levels are only slightly elevated.
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PMID:Secretin-stimulated serum gastrin levels in hyperparathyroid patients from families with multiple endocrine adenomatosis type I. 1 40

H+ secretion and gastrin concentration were measured before and after electric vagal stimulation during proximal selective vagotomy in 29 patients with duodenal ulcers. Before vagotomy, H+ secretion and serum gastrin concentration significantly rose after stimulation, while after complete vagotomy H+ secretion remained below basal values, although serum gastrin concentration was significantly increased. These results indicate that without vagal innervation there is no gastrin secretion within physiological levels. The method is suitable for testing the completeness of the vagotomy, the results not agreeing with those obtained by pressure measurements (Burge's method).
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PMID:[Stimulation of H+ secretion and serum gastrin by intra-operative electrical vagal stimulation before and after proximal selective vagotomy (author's transl)]. 1 36

The role of secretin in the postprandial bicarbonate response by the pancreas is not clear. This study reports secretin and bicarbonate secretion after exogenous and endogenous acidification of meal. In dogs with gastric and pancreatic fistulas, a liver extract meal at various pH levels was introduced into the stomach and kept at the preselected pH by intragastric titration. Gastric acid, pancreatic bicarbonate, serum gastrin, and plasma secretin were measured. The meal at pH 7 produced an increase of gastrin levels of 230% above basal and a gastric acid output from a basal of 0.8-16.9 meq/30 min. Acidification of the meal evoked a pH-dependent reduction of gastrin and gastric acid secretion, a pH-dependent elevation of pancreatic bicarbonate, and significant elevation of secretin at pH 3 (43% above basal) and at pH 2 (80% above basal). Postprandial endogenous acidification of a meal, without intragastric titration, also provoked significant release of secretin. Maximal pancreatic bicarbonate secretion in response to exogenous secretin was augmented 30% by the addition of a liver extract meal at pH7. It is concluded that in dogs with pancreatic fistulas, a meal exogenously or endogenously (postprandial) acidified is capable of the release of secretin in immunoassayable amounts. The normal pancreatic bicarbonate response to food may depend partially upon potentiation of the secretin effect by other neurohumoral stimuli.
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PMID:Pancreatic bicarbonate, serum gastrin, and secretin responses to meals varying in pH. 1 21

The effects of gastrin on the cell kinetics of the gastric mucosa were studied in the rats. The labelling index by tritiated thymidine of the cell in the mucous neck zone began to rise 14 hours after a single dose of tetragastrin at 100 or 1,000 microgram/kg or synthetic human gastrin at 1,000 microgram/kg and reached the peak at 18 hours. With tetragastrin 100 microgram/kg administered subcutaneously together with a depot for 35 days, observations were made on the change in the turnover rate of the gastric epithelium by means of labelling index. The turnover rate was delayed in the surface epithelium and accelerated in the cells at the lower part of the foveolae in the gastrin-administered group. The cell suspension prepared from the rat gastric mucosa by trypsin digestion was cultivated with 5 per cent of CO2 in air for 48 hours. The group which was added with 10 microgram/ml of tetragastrin showed fluctuations in the labelling index almost similar to the groups administered 100 and 1,000 microgram/kg in vivo. It might be possible to support the hypothesis that gastrin not only has a trophic effect on the mucous neck zone but it also might be concerned with the turnover of the mature stage of gastric mucosa.
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PMID:Effect of gastrin on the cell kinetics of rat gastric mucosa. 1 92

The influence of a coffee-antazid-mixture was investigated at 30 patients with diseases of the stomach (17 with duodenal ulcer, 6 with gastric ulcer and 7 with chronic gastritis) in comparison to a commercial coffee. The parameters measured were the gastric basal acid output, the continuous registration of the pH by an intragastric electrode and the serum gastrin concentration before and after the application of the tests substances. 75% of the patients with duodenal ulcer showed a positive effect by means of a greater elevation of the intragastric pH after application of the mixture in comparison to coffee. The effect was strongly correlated to the basal acid ouptput. In the group with gastric ulcer and that with duodenal ulcer under the influence of the mixture the pH after the initial rise decreased to less deeper values. There was a close relationship to the patterns of gastric ulcer as well with chronic gastritis there was an additional facourable effect on the symptoms of abdominal pain which occured after coffee and not after the mixture. The group with chronic gastritis showed no difference between the pure coffee and the coffee-antacid-mixture. A possible relationship of the products of coffee roasting and the adsorptive properties of the antacid is discussed.
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PMID:[Effects of a coffee-antacid-mixture and a commercial coffee with regard to gastrin, pH and gastric secretion (author's transl)]. 1 88

In the course of investigations of gamma-oryzanol in rats, circadian rhythms in antiulcerogenic action on gamma-oryzanol were observed. Circadian rhythms in several other parameters were investigated and correlated with the antiulcerogenic action. Pretreatment of rats with gamma-oryzanol 100 mg/kg, s.c., for 5 days tended to decrease serum gastrin levels and gastric secretion, and to increase serum 11-OHCS. Suppresive patterns of serum gastrin and gastric secretion following the pretreatment with gamma-oryzanol corresponded to the circadian rhythms in antiulcerogenic action of gamma-oryzanol. A complication of our results suggests that increment of catecholamines in rat brain after gamma-oryzanol plays a role in the above mentioned actions.
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PMID:[Studies on gamma-oryzanol. III. Influence of gamma-oryzanol on circadian rhythms of serum gastrin, 11-OHCS and gastric secretion in rats (author's transl)]. 2 Mar 95

Tests staged on dogs demonstrated the action of GMP to differ depending upon the nature of the gastric secretion stimulant actually used. The inhibition of the gastric juice secretion occurring against the background of multiple introduction of histamine or gastrin tetrapeptide amide was quite spectacular: the secretion dropped down to zero and the action was more prolonged than following administration of pentagastrin with which the secretion was not inhibited to such a sharp degree and the effect of GMP was less protracted. The mechanism of the GMP action of the gastric secretion and the causes of described differences require further investigations.
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PMID:[Inhibiting action of glycomacropeptide on stomach secretion induced by various humoral stimulants]. 2 Jun 92

By arranging a series of psychological contingencies (unpredictability, uncontrollability, conflict), coupled with delivery of a physical stimulus (electric shock), we produced gastroduodenal mucosal lesions in 7 of 8 rhesus monkeys. The most severe conflict paradigm most consistently produced lesions across subjects. Of the 30 lesions observed by endoscopy, 80% occurred near the anatomic junction of gastric body and antrum, in the antrum, or in the duodenum. Lesions varied in severity from discolorations of the mucosa to disruptions of mucosal integrity. Lesions in the stomach generally disappeared in several days despite the continuation of stress; some duodenal lesions were equally evanescent, but in 2 monkeys, lesions lasted over a week. Hydrogen ion kinetics were measured in 2 monkeys that developed gastric lesions and 2 that developed duodenal lesions. The rate at which hydrogen ion entered the duodenum was uniformly suppressed for all 4 monkeys during their first session of shock avoidance; during their last session, the gastric subgroup continued to show suppression while the duodenal subgroup returned towards control levels. Serum gastrin levels were unchanged by the multiple-stress procedures. Our finding of consistently producible, stress-induced gastroduodenal pathology in anatomic areas similar to those involved in man suggests that the subhuman primate is suitable for further efforts to produce an animal model of psychosomatic ulcer disease.
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PMID:Effect of multiple-stress procedures on monkey gastroduodenal mucosa, serum gastrin, and hydrogen ion kinetics. 2 64


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