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)

To examine the relative importance of calcium and gastrin in regulation of calcitonin secretion, we administered graded oral doses of calcium to 10 normal men, ages 23-29 yr. Each subject had previously shown an appropriate increase in calcitonin secretion in response to a pharmacologic (0.5 mug/kg) pentagastrin injection. On separate days and in random order, each man drank 250 ml of distilled water containing 0.0, 0.5, 1.5, and 3.0 g of elemental calcium as the gluconate salt. Blood samples were drawn before and at 30, 60, 90, 120, 180, and 240 min after the oral calcium dose. The samples were analyzed for calcium by atomic absorption spectroscopy, and for gastrin and calcitonin by radioimmunoassays of established sensitivity and specificity. Ingestion of water (control) caused no change in any of the three variables. Calcium ingestion resulted in dose-related increases, within the normal range, of all three variables. Immunoreactive gastrin rose promptly, peaking at 30 min, and returning to basal levels or below by 120 min. In contrast, calcium and immunoreactive calcitonin levels rose slowly and in parallel, peaking at 120-240 min. Changes in calcitonin and changes in calcium were strongly and positively correlated, r = 0.73, when all data were pooled. Furthermore, individual linear regressions for changes in calcitonin and calcium levels (calculated separately for the three oral calcium doses in each subject) had positive slopes in 28 out of 30 sets (P < 0.01). The changes in calcitonin concentrations were much more poorly correlated with the corresponding changes in serum gastrin levels; in fact, the regression coefficient was weakly negative, r = -0.20. These results show that, at least in young adult men, changes of ambient calcium concentration within the normal range may be of major importance in physiologic regulation of calcitonin secretion. The findings are consistent with the hypothesis that calcitonin functions to prevent excessive postprandial hypercalcemia.
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PMID:Regulation of calcitonin secretion in normal man by changes of serum calcium within the physiologic range. 50 Aug 34

The suppressive effect of histamine H2-receptor antagonist, cimetidine, on gastric secretion was investigated in Ghosh-Schild rat. The study above was done in basal state under infusing normal saline (1 ml/h) and stimulated state by histamine-di-chloride (3.5 mg/kg-h), tetragastrin (50 mcg/kg-h) or calcium chloride (4 mg/kg-h). Dose related increase of cimetidine (1.7, 3.5, 7.0 and 14.0 mg/kg-h) were observed and correlated with the degree of inhibition of acid secretion. Cimetidine had a potent inhibitory activity on either basal and stimulated acid output by the agents above. Basal acid secretion was completely abolished by 3.5 mg/kg-h of cimetidine to the level of anacidity. The degree of inhibition by the same dose of cimetidine was different among the agents used as stimulant on acid secretion and it followed in the order of calcium, gastrin and histamine subsequently. This study indicated that histamine H2-receptor participated the gastric secretion induced by either gastrin or calcium other than histamine itself. This fact indicated the important role of endogenous histamine in gastric secretion induced by calcium and gastrin.
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PMID:An experimental study on histamine H2-receptor antagonist on calcium, gastrin and histamine induced gastric acid secretion in rat. 52 95

In order to investigate the frequency of fasting hypergastrinaemia in primary hyperparathyroidism (A) and in chronic hypercalcaemia (B), in 40 and 16 patients respectively gastrin, parathyroid hormone (PTH) and serum calcium levels were measured and compared with those of a control group (40 subjects) with similar distribution of sex and age. Moreover, possible linear relationships between these parameters were investigated. Notwithstanding significant differences in calcium and PTH levels between the three groups (A: high PTH, high Ca++; B: low PTH, high Ca++; C: normal PTH and Ca++ levels), no significant difference in gastrin levels were found. However, in the first group, a marked increase of gastrin was observed in one patient, very probably affected by a gastrin-secreting tumor (positive secretin test). While no linear relationship between PTH and gastrin values was present in all the three groups, a significant correlation between serum calcium and fasting gastrin was detectable in the group A, ruling-out the above mentioned patient. Present data suggest that PTH does not modify gastrin levels and that chronic moderate hypercalcaemia does not raise serum fasting gastrin, at least in clinical conditions. Moreover, the frequency of hypergastrinaemia in hyperparathyroidism is very low and it seems to be present only in patients with gastrin-secreting tumors.
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PMID:Fasting serum gastrin in primary hyperparathyroidism and in chronic hypercalcemia. 54 29

The effect of induced hypercalcemia on serum gastrin concentrations, measured by radioimmunoassay, and gastric acid secretion was studied in 20 healthy subjects, 8 patients after antrectomy and gastroduodenostomy (Billroth I), 12 patients after antrectomy and gastrojejunostomy (Billroth II) and in 9 patients after total gastrectomy and esophagojejunostomy. In normal man calcium stimulates gastric secretion and gastrin release. After antrectomy gastric secretion is still stimulated by calcium without changing serum gastrin levels. After total gastrectomy basal serum gastrin concentration is further reduced; calcium does not liberate gastrin. These results show that calcium-induced gastric secretion is caused by direct action at the parietal cell level besides the gastrin release from the antrum. In man, extra antral gastrin cannot be released by induced hypercalcemia.
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PMID:[The effect of antrectomy or total gastrectomy on calcium-induced gastrin secretion and gastrin release in man (author's transl)]. 59 73

Bombesin caused depolarization of rat or mouse pancreatic acinar cell membrane, reduction of membrane resistance, and a steep rise in amylase output from superfused pancreatic fragments. These effects were similar to those previously described for acetylcholine, cholecystokinin, and gastrin. The dose-response curves for these three effects of bombesin were very similar, with effects being detectable at concentrations of about 30 pM and maximal effects at about 10 nM. The equilibrium potential for the membrane action of bombesin, i.e., the membrane potential at which bombesin did not cause any change in membrane potential, was -16 mV. Similar values for equilibrium potential were obtained with acetylcholine, caerulein and pentagastrin. Bombesin in the higher dose range (10 nM) caused electrical uncoupling of acinar cells within an acinus, i.e., a marked increase in junctional membrane resistance. Similar uncoupling effects were observed after acetylcholine, caerulein, and pentagastrin stimulation. In conclusion, bombesin acts on the pancreatic acinar plasma membrane in exactly the same way as acetylcholine and cholecystokinin-pancreozymin. The electrical uncoupling caused by stimulation is evidence for an increase in cytosol free calcium ion concentration.
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PMID:In vitro action of bombesin on amylase secretion, membrane potential, and membrane resistance in rat and mouse pancreatic acinar cells. A comparison with other secretagogues. 61 13

Recurrent peptic ulcer usually develops as the result of an ill-advised or poorly executed operation. The commonest surgical error is an incomplete vagotomy. Diagnosis is made best by endoscopy. Mandatory investigation includes determination of serum gastrin and calcium, and measurement of basal and maximal acid output. Management is surgical and depends on the initial ulcer operation. Decision-making is aided by the Hollander insulin test, the secretin infusion test and occasionally by a technetium scan. There is no place for procedures that do not reduce acid output. Emergency treatment of a complication should be followed by full investigation and the appropriate operation. Recurrent gastric ulcer should be treated by gastrectomy and excision of the ulcer.
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PMID:Symposium on peptic ulcer disease: 3. Practical management of recurrent peptic ulcer. 62 Mar 62

The effects of calcium and secretin were studied in 8 patients with the Zollinger-Ellison syndrome and 18 patients with duodenal ulcer disease. Intravenous infusion of calcium gluconate produced marked increases in serum gastrin levels in the patients with Zollinger-Ellison syndrome (4,350 +/- 1,625 pg/mg) and very slight increases in the patients with duodenal ulcer disease (140 +/- 49 pg/ml). Secretin given as a single intravenous injection also induced marked elevations in serum gastrin in the group with the Zollinger-Ellison syndrome (4,063 +/- 1,990 pg/ml). By contrast, intravenous secretin resulted in a progressive fall in serum gastrin levels in the duodenal ulcer group (from 119 to 97 pg/mg). These results suggest that both stimuli are very useful dagnostic tools in discriminating between Zollinger-Ellison and non-Zollinger-Ellison patients. The secretin challenge test is felt to be superior to the calcium infusions because it is simpler, safer and very rarely produces false-negative or-positive results.
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PMID:Calcium and secretin as provocative stimuli in the Zollinger-Ellison syndrome. 62 16

Retained gastric antrum was evaluated in six dogs, and diagnostic methods correlated with histopathology. Secretin and calcium infusion did not significantly alter circulating gastrin levels. 99 mTc scanning was uniformly positive and did not depend on the presence of parietal cells. The failure to consistently develop hypergastrinemia and the absence of gastrin cell hyperplasia suggest that factors other than gastrin may be implicated in the recurrent ulceration seen with retained antrum.
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PMID:Experimental retained antrum. Diagnostic technics and histopathologic correlations. 64 42

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

Prostaglandin E1, while inhibiting gastric fistula and Heidenhain pouch acid output in the dog, did not inhibit gastrin released by acetylcholine irrigation of an isolated antral pouch independent of pH effect. Some increase in gastrin was noted to PGE1 against a background of calcium infusion and following a meal. This increase is presumably due to acid inhibition and to an increase in intraluminal pH.
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PMID:Prostaglandin E1 inhibition of acid but not gastrin. 69 12


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