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)

Both vagal and sympathetic innervation been have described as influencing hormone release from the gastrointestinal tract and pancreas. The role of neural influences on the release of gastrin, glucagon, and secretin has been studied using the potent autonomic nerve stimulus of hypoglycaemia. Healthy subjects were each rendered hypoglycaemic by insulin 0.2 units/kg on three occasions: after atropine 20 microgram/kg: after propranolol 160 mg orally, and without prior drug administration. Adequate beta-blockade was confirmed by observation of the pusle rate response to a standard exercise at the end of the experiment, and by measurements of plasma propranolol levels. Hypoglycaemia failed to produce a rise in plasma gastrin under either propranolol or control conditions but a significant rise was noted with prior atropinisation. The glucagon response to hypoglycaemia, when measured with either the C- or N-terminal reactive antibodies, was found not to be influenced to any significant extent by either beta-blockade or atropinisation. No alteration in plasma secretin levels was noted during hypoglycaemia. It therefore appears that neural influences are relatively unimportant in the release of gastrin, glucagon, and secretin in man.
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PMID:Role of neural influences in the release of gastrin, glucagon, and secretin during hypoglycaemia in man. 68 May 95

The effect of dopamine infusion on basal and pentagastrin-stimulated gastric secretion, on basal and secretin-CCK-PZ-stimulated pancreatic secretion, and on basal and meal-induced gastrin release has been evaluated in healthy volunteers. Both basal and stimulated gastric acid secretion were significantly inhibited during dopamine infusion with a significant rebound to pre-infusion values after discontinuing dopamine. These effects were prevented by pretreatment with the antidopaminergic drug, metoclopramide. A slight but now significant decrease in amylase and bicarbonate outputs was also observed during dopamine infusion, while gastrin release did not change. These data suggest the existence of dopaminergic mechanisms in the regulation of gastric acid secretion in man.
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PMID:Effect of dopamine infusion on gastric and pancreatic secretion and on gastrin release in man. 68 Jun 4

The effects of recent diagnostic and therapeutic advances were assessed in 65 patients with the Zollinger-Ellison syndrome (ZES). Twenty-seven patients seen between 1955 and 1970 were compared with 38 patients seen between 1971 and 1977. The earlier patients had a higher incidence of virulent ulcer disease (56% vs. 24%), other endocrinopathies (48% vs. 13%), and malignant gastrinoma (44% vs. 25%). Earlier diagnosis is the result of liberal use of serum gastrin measurements and provocative tests for gastrin release (calcium and secretin), and an increased awareness of this syndrome. Because their basal gastrin values were in a range that overlapped ordinary ulcer disease, 47% of patients encountered in recent years required provocative testing with secretin for diagnosis. If the gastrin concentration falls to normal following resection of a gastrinoma, the tumor has probably been completely removed. In our patients, gastrin measurements after total gastrectomy had no prognostic significance in regards to clinical progression or regression of the neoplasm. Of 12 patients treated with cimetidine, nine experienced symptomatic improvement, and three did not. Resection of the gastrinoma should be attempted if the lesion is solitary and located in the body or tail of the pancreas, or if it is an isolated duodenal lesion. Otherwise, total gastrectomy remains the treatment of choice. In 38 patients, total gastrectomy with Roux-en-Y esophagojejunostomy was followed by 97% survival and minimal difficulties with nutrition or dumping.
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PMID:The Zollinger-Ellison syndrome--23 years later. 68 1

A case of recurrent duodenal ulcer, basal gastric hypersection, and hypergastrinemia of antral origin is presented. The diagnosis was suggested preoperatively by stimulation tests with secretin and food. Billroth II antrectomy led to normalization of serum gastrin within half an hour. The gastrin content of the antral mucosa was not increased, neither was antral G-cell hyperplasia demonstrable. Postoperatively the basal gastric acid output and fasting serum gastrin levels were normal, without a postprandial increase in serum gastrin concentrations. The case does not support the existence of a specific disease called antral G-cell hyperplasia.
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PMID:Hypergastrinemia of antral origin in duodenal ulcer. 71 63

Continuous treatment of three Zollinger-Ellison patients with histamine H2-receptor antagonists for 14, 26 and 31 months resulted in effective relief of complaints and marked reduction in gastric acid secretion. In one of the patients the dose of cimetidine had to be doubled after 15 months of treatment because of a rise in basal gastric acid secretion accompanied by recurrent diarrhea. Fasting and secretin-stimulated serum gastrin levels were not affected by long-term treatment with histamine H2-receptor antagonists. No side-effects were observed in the three patients on long-term treatment.
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PMID:Long-term treatment with histamine H2-receptor antagonists in Zollinger-Ellison syndrome. 71 79

Recently attempts have been made to demonstrate the possible role of hypergastrinemia in the production of congenital hypertrophic pyloric stenosis in infants. Eleven infants with congenital hypertrophic pyloric stenosis, ranging in age from three to 11 weeks, were evaluated for fasting and postprandial serum gastrin levels. Two to ten weeks following successful pyloromyotomy, a similar evaluation was undertaken to demonstrate the possible role of elevated serum gastrin levels in the etiology of congenital hypertrophic pyloric stenosis. The average fasting and postprandial serum gastrin levels in infants with congenital hypertrophic pyloric stenosis did not differ significantly from levels noted in control infants. Similarly, no statistically significant difference was noted between the pre- and postoperative levels of serum gastrin in the affected infants. Several experimental studies have been reported within the past few years describing the production of hypertrophic pyloric stenosis in the offspring of dogs injected with pentagastrin during pregnancy. The results of our study minimize the direct importance of serum gastrin in the production of congenital hypertrophic pyloric stenosis. The role of the hormone secretin in the etiology of this condition is hypothesized.
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PMID:Fasting and postprandial serum gastrin levels in infants with congenital hypertrophic pyloric stenosis. 71 86

Antibody was readily produced in a rabbit against synthetic porcine secretin coupled to BSA. The final dilution of the antiserum to bind 50% of 1 fmol 125I-labeled secretin was 1 : 150,000. The effective equilibrium constant (Keff) according to Scatchard was 3.4 X 10(11) l/mol, the average equilibrium constant (Ko) according to Sips 3.5 X 10(11) l/mol, and the index of heterogeneity (alpha) according to Sips 1,00. No cross reactivity was found for gastrin, glucagon and insulin. 125I-labeled synthetic porcine secretin was prepared by the Chloramine-T-method, and the label purified on a Sephadex G-15 column followed by a SP Sephadex C-25 column had a specific radioactivity of 1.150 muCi/nmol. The radioimmunoassay method described has a detection limit of 1.6 pmol/l with 95% confidence limit, a within assay precision of 9,6%, and a between assay precision of 12.8%. It allows detection of fasting plasma secretin in the low pmol/l range, and the rather sharp rise and fall in plasma secretin subsequent to a brief period of duodenal acidification. The problem involved in measuring plasma secretin have been overcome by acidification of the plasma, and by subtracting the "apparent" secretin concentration in corresponding secretin-free plasma prepared by incubation at 37 degrees C for 96 h for each subject.
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PMID:Radioimmunoassay of secretin in acidified plasma. 72 17

Fasting levels of 5 gut hormones were studied in 30 patients with advanced uraemia (CRF), 40 undergoing regular dialysis (RD) and 555 renal transplant patients (RT). Mean values of gastrin and total glucagon were markedly elevated in CRF and RD patients compared with 20 normal subjects; there were lesser elevations in pancreatic glucagon, insulin and vasoactive intestinal peptide (VIP). Secretin levels were unchanged. In RT patients, fasting levels of VIP and pancreatic glucagon had returned to normal, while levels of gastrin, total glucagon and insulin remained slightly elevated compared with controls. Food stimulated hormone levels were measured in 18 RD patients and compared with 18 controls. After eating, RD patients failed to show the late increase in total glucagon, or the suppression of VIP and secretin seen in normal subjects; the pattern of gastrin and insulin response was similar to controls, but after the initial increase plasma levels in RD patients tended to show a slower decline. Thus involvement of the gastrointestinal tract in uraemia is associated with functional disturbance of the endocrine system of the gut.
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PMID:Elevations of gastrointestinal hormones in chronic renal failure. 74 Jun 78

Abnormal acid production or handling is thought to be involved in duodenal ulceration. Gastric emptying of 25 mmol hydrochloric acid (250 ml 0.1 M solution) was studied by using an isotopic method in control and ulcer subjects. Plasma gastrin and secretin levels were simultaneously measured. Gastric emptying was significantly faster in ulcer subjects using several parameters. Plasma gastrin levels were suppressed in both groups, with equivocal differences between them. Mean plasma secretin levels showed no significant elevation in controls and at only one point in ulcer subjects. Mean elevation in plasma secretin levels during intermediate phase of gastric emptying (T30-70) correlated with rate of acid loss from stomach in both groups. Regression lines were significantly different in position, however, and indicated a higher threshold for secretin release in ulcer subjects. The significance of this in the pathogenesis of duodenal ulcer is discussed.
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PMID:Gastric emptying of ingested acid and its effects on plasma gastrin and secretin in duodenal ulcer subjects. 75 76

VIP and secretin were compared in regard to their effects on gastric acid and pepsin secretion induced by pentagastrin histamine or a peptone meal as well as on gastric mucosal blood flow and meal induced serum gastrin level in conscious dogs provided with gastric fistulas and denervated fundic pouches. Both VIP and secretin caused a dose-related stimulation of basal pepsin outputs and inhibition of pentagastrin-induced acid secretion. VIP, like secretin, inhibited pentagastrin and meal-induced gastric acid secretion but in contrast to secretin it caused inhibition of acid response to histamine. Inhibition of acid secretion by VIP or secretin was accompanied by secondary reduction in gastric mucosal blood flow in tests with pentagastrin or histamine and by depression of the serum gastrin level in tests with a peptone meal. This study indicates that in comparison with secretin, VIP has a wider spectrum of inhibition of stimulated gastric secretion and may be considered as one of the enterogastrones released in the small intestine.
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PMID:Comparison of vasoactive intestinal peptide (VIP) and secretin in gastric secretion and mucosal blood flow. 76 58


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