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)

In addition to established gastrointestinal hormones--secretin, cholecystokinin-pancreozymin (CCK-PZ), gastrin, and glucagon---some 30 polypeptides with gastrointestinal actions can be listed. New aspects of these substances include the following: Gastrin and vasoactive intestinal peptide (VIP) can be also encountered in the central nervous system and may act as transmitters. CCK-PZ-serum concentrations are found markedly elevated in patients with exocrine pancreatic insufficiency; this may provide the opportunity to establish a realtively simple screening test. Moreover, there is evidence that serum-CCK-PZ levels serve as satiety signal. Secretin secretion is said to be enhanced in hunger and then to act as a lipolytic hormone. In addition to enteroglucagon, a gastrintestinal peptide identical to pancreatic glucagon has been detected. Gastric inhibitory polypeptide (GIP) inhibits gastric secretion and motility (enterogastrone activity) and together with glucose it stimulates insulin release (incretin activity). Motilin increases lower esophageal sphincter pressure, enhances gastric pepsin secretion and slows down gastric evacuation. Serum levels of pancreatic polypeptide may be found elevated as a diagnostic index in patients with endocrine peptide tumors of the pancreas. Recently, the potential importance of local (paracrine) actions of gastrointestinal polypeptides has been amphasized. Predominantly paracrine activity is exhibited by some prototype hormones, e.g. somatostatin, substance P, bombesian, and the non-polypeptide compounds, prostaglandins.
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PMID:[New views on gastrointestinal hormones]. 85 99

The inhibitory actions of intravenous somatostatin on the gastric secretory responses to pentagastrin (1.5 microng/kg-h i.v.) and to a meal (10% peptone, pH 5.5) were studied in six healthy subjects. Meal-induced gastric acid output was estimated by means of a modified Fordtran and Walsh method of intragastric titration. Somatostatin (5 microng/kg-h; cyclic form) significantly inhibited the total 1-hour acid response to pentagastrin by about 70% (inhibition of pepsin secretion: about 70%) and that to a test meal by about 75%. During the last 30 min of somatostatin infusion the pentagastrin-stimulated secretion of acid was significantly reduced by about 90% (inhibition of pepsin output: about 85%) while the corresponding figure in the test with meal-induced secretion was about 95%. Serum gastric--elevated in response to the test meal--was found to be merely lowered by about 30% during somatostatin infusion. Consequently, it is tempting to assume that inhibition of human gastric acid secretion by exogenous somatostatin largely results from a direct antisecretory effect upon parietal cells and, only to a minor extent, from an indirect action via reduction of gastrin release.
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PMID:Inhibition by somatostatin of gastrin release and gastric acid responses to meals and to pentagastrin in man. 86 87

A Levine tube was placed under radiological control in the stomach, and a thin polyethylene tube in the proximal jejunum of 6 healthy volunteers. The stomach and proximal part of jejunum were perfused for 2 hours with 1% acetylcholine, 20% meat extract (Bovril), and 15% liver extract (LE) alone and in combination with simultaneous infusion of different doses of exogenous pentagastrin intravenously. A significant increase in serum gastrin concentration was found with antral perfusion of LE only, whereas perfusion of the proximal jejunum did not change the basal level of the serum gastrin concentration. No change from control values was observed in gastric acid, and pepsin output on perfusing proximal jejunum with LE alone, or in combination with pentagastrin. Reflux to the stomach varied between 0-1.4%, as determined by addition of radioactive B12 to the perfusates. The experiments showed that gastrin was released from the antrum of the stomach by perfusion with 15 per cent LE, but not from the jejunum under the present experimental conditions. In the present experiments Bovril and acetylcholine perfusions did not cause significant responses from the antrum or from the proximal jejunum.
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PMID:The intestinal phase of gastric secretion. Response to liver extract infusion into the proximal jejunum of healthy human subjects. 93 4

1 The effect of isoprenaline on gastric secretion evoked by various means has been studied in conscious rats provided with Pavlov and Heidenhain pouches. 2 Interdigestive acid secretion in the Pavlov pouch was reduced by isoprenaline, whereas pepsin secretion was unaltered. 3 Central vagal stimulation effected by 2-deoxy-D-glucose injection evoked a gastric secretory response that was substantially reduced by isoprenaline. 4 2-Deoxy-D-glucose increased the mobilization of gastric mucosal histamine, an effect that was prevented by isoprenaline. 5 Isoprenaline infusion alone induced a slight increase in histamine mobilization and also a considerable elevation of immunoreactive serum gastrin concentration. 6 The secretory response to food in the Pavlov pouch was almost abolished by isoprenaline. 7 Although the acid response to histamine in the Heidenhain pouch was susceptible to isoprenaline inhibition, that to methacholine was not. 8 Pepsin secretion in the Heidenhain pouch preparation stimulated by histamine or methacholine seemed to be enhanced by isoprenaline.
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PMID:Further studies on the mode of action of isoprenaline on gastric secretion in the conscious rat. 97 74

1) In chronic gastric ulcer bed rest, leaving out smoking and carbenoxolone have increased the rate of healing. 2) In chronic duodenal ulcer it has yet to be shown that any medical measure so far significantly altered the course of the disease. 3) The surgical approach to the treatment of chronic duodenal ulcer is based upon three principles, all of them aiming at reducing the acid-pepsin secretion: a) Removal of the acid secreting mucosa decreases the acid secretory capacity of the stomach; b) Removal of the pyloric antrum eliminates the main source of gastrin, the major known humoral excitant of acid secretion; c) Section of the vagi probably renders the acid secreting cells less responsive to humoral stimulation (Brooks). The major problem, however, which is the prevention of recurrent duodenal ulcer is yet unsolved. There is some hope that the new receptor blocking agent metiamid is the first step, and there is even more hope in that the proceedings of this symposium will show us further steps forward.
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PMID:The rationale in the treatment of peptic ulcer disease. 97 73

Current concepts on the pathophysiology of gastric hypersecretion in duodenal ulcer disease have been presented and the role of vagal nerves and gastrointestinal hormones particularly gastrin has been discussed. Duodenal ulcer patients form a heterogenous group with regard to the gastric acid and pepsin secretion and gastrin release. They may differ from healthy subjects by several wall defined defects including an increased mass of parietal and peptic cells, increased capacity to secrete acid and pepsin, increased vagal drive to the parietal cells, hyperreactivity of antrum, decreased effectiveness of antral and duodenal autoregulatory mechanisms, defective release of secretin, increased gastric emptying and defective removal of gastric acid load from the duodenum. Very little is known what proportion of duodenal ulcer patients suffer from various pathologic disturbences and what are the mechanisms underlying these changes.
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PMID:Vagal and hormonal influences on gastric secretion in duodenal ulcer disease. 98 32

Gastric secretion was studied in 188 fetuses of 28 pregnant dogs near term. Baseline secretory values were determined and gastric secretion was stimulated in additional fetuses with histamine, insulin, or gastrin. A significant increase in volume, acidity and pepsin output was observed in fetuses stimulated during the last week of gestation. Following maternal stimulation the placental transfer of histamine, insulin, and gastrin are demonstrated.
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PMID:[Animal-experiment studies on the pathogenesis of peptic ulcer in the newborn]. 103 12

The effect of glucagon on gastric acid and pepsin secretion, basal or stimulated by a meal, pentagastrin and histamine, was studied in duodenal ulcer patients. Intravenous glucagon infused in graded doses ranging from 6.2 to 50 mug per kg-hr produced a dose-related inhibition of pentagastrin-induced acid secretion reaching about 40% of the control level at the dose of 50 mug per kg-hr. Acid inhibition was paralleled by a decrease in the pepsin output and serum calcium level and was accompanied by a rise in the blood glucose concentration. Glucagon used in a standard dose of 25 mug per kg-hr produced about 50% inhibition of acid secretion induced by a meal (measured by intragastric titration) accompanied by a significant decrease in the serum gastrin level measured by radioimmunoassay. Histamine-induced secretion was only slightly inhibited by glucagon, and the degree of inhibition for acid (25%) and pepsin (20%) secretion was statistically insignificant.
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PMID:Effect of glucagon on meal-induced gastric secretion in man. 108 77

Antrocolic transposition in four dogs with Heidenhain pouch and gastrojejunostomyresulted in a marked increase in fasting plasma gastrin concentration and sustained highacid secretion, closely related to gastrin levels. A marked production of pepsin output could not be correlated with plasma gastrin. Reduction in plasma gastrin concentration was more than twofold less pronounced than the reduction in acid output for 1 and 2 U/kg-h, while the 0.5 U/kg-h no effect was noted. For both acid output and gastrin concentrations, close correlations were noted between presecretion level and remaining level upon secretin infusion. Despite the reduction in the secretory volume of the pouch, 0.5 and 1 U/kg-h of secretin induced a 1.5- and 2-fold increase in pepsin output, respectively. Two untis per kilagram-hour decreased the secretory volume as well as the pepsin output. If the physiological release of secretin in dogs does not exceed the equivalent of the lowest dose studied, our results would indicate that acid inhibition is a physiological activity of secretin, while the effect on circulating gastrin concentration seems to be phamacological.
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PMID:Secretin effect on gastrin, gastric secretion in dogs with chronic antral stimulation. 109 82

Heidenhain pouches were established in four mongrel dogs. Acid secretory values were studied in response to a meal, both after operation and six to eight months later. Large increases in the acid responses of the Heidenhain pouch to a meal were noted over a period of time. Mechanisms accountable for this acid increase were studied, including serum gastrin response, pepsin activity, and morphologic changes in the pouch. Regeneration or reinnervation of vagal fibers may occur at a subthreshold level but is not well documented. The necessity of repeated control studies in long-term evaluation using the Heidenhain pouch is emphasized.
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PMID:Increasing acid response to a meal in the chronic Heidenhain pouch. 110 17


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