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Query: UNIPROT:P01350 (gastrin)
 9,683 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have compared the effects of oral and intravenous ethanol on the secretion of both thyrocalcitonin and gastrin in five patients with medullary carcinoma of the thyroid. Ethanol caused a moderate rise in plasma thyrocalcitonin to 316% +/- 343% of baseline when given intravenously and to 197% +/- 106% of baseline when given orally. Only oral ethanol caused a measurable rise in serum gastrin levels. Serum calcium did not change significantly from baseline during either oral or intravenous administration. The results suggest that stimulation of thyrocalcitonin secretion by ethanol is not secondary to increased secretion of gastrin nor to the induction of hypercalcemia. Neither oral nor intravenous ethanol appears to be as effective as intravenous pentagastrin in testing for the presence of medullary carcinoma.
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PMID:Stimulation of thyrocalcitonin secretion by ethanol in patients with medullary thyroid carcinoma--an effect apparently not mediated by gastrin. 118 95

In 36 patients with ulcer without Zollinger-Ellison-syndrome (25 patients with recurrent duodenal ulcer, 11 with an ulcus pepticum jejuni after B II-resection of the stomach) and 2 patients suffering from ulcus pepticum jejuni with an ascertained gastrinoma the secretion of acid was compared after stimulation of pentagstrin (6 mug/kg) and calcium (4 mg Ca++/kg/h). The secretion of hydrochloric acid was statistically significantly stimulated in all patients suffering from ulcer by the hypercalcaemia (increase of the serum calcium concentration from 5.0 +/- 0.3 mval/1 to 6.2 +/- 0.8 mval/1). But in patients suffering from ulcer with gastrinoma the stimulatory effect was larger than in such patients without autonomous source of gastrin: the calcium-stimulated secretion of hydrochloric acid was on the average in cases of duodenal ulcer 40% (2 to 68%), in the ulcera peptica jejuni 47% (17 to 75%), in the 4 comparative examinations of the two patients with Zollinger-Ellison-syndrome, however, always more than 100% (106 to 177%) of the pentagastrin-stimulated peak secretion. The comparative test of the pentagastrin and calcium-stimulated secretion of hydrochloric acid could be a help for the proof of autonomous places of the formation of gastrin.
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PMID:[Influence of an acute hypercalcemia on the gastric secretion in duodenal ulcer, peptic ulcer of the jejunum and Zollinger-Ellison syndrome]. 119 39

These studies show that calcium stimulates gastric secretion and gastrin release in healthy individuals and duodenal ulcer patients. After antrectomy calcium still stimulates gastric secretion without affecting basal serum gastrin concentration. After total gastrectomy serum gastrin levels are decreased; hypercalcemia results in a small but definite release of gastrin from extraantral sites.
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PMID:[Effect of antrectomy of total gastrectomy on calcium-induced gastric secretion and gastrin liberation in man]. 120 39

1. In a preopertive group of patients suspected of having the Zollinger-Ellison syndrome the serum gastrin and gastric acid response to calcium infusion may be highly diagnostic. 2. In a group of Zollinger-Ellison syndrome patients following total gastrectomy, the gastrin response to calcium infusion correlates well with presence or absence of tumor.
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PMID:Calcium infusion test before and after total gastrectomy in the Zollinger-Ellison syndrome. 121 33

In healthy controls (n = 7), patients with duodenal ulcer (n = 7), primary hyperparathyroidism (n = 7), and 1 case of excluded gastric antrum the effects of intravenous secretin ("Karolinska"; 3 U/kg/h for 90 min) upon serum calcium fractions, total protein, and the integrated response of gastrin and glucagon were investigated. In all groups total calcium, total protein, and protein-bound calcium fraction rose significantly but the inonized calcium fraction remained stable. Since serum concentration of gastrin and glucagon could not be altered in any of the groups a direct interference of these hormones with calcium homeostasis during secretin infusion can be ruled out. Hyperparathyroid patients had higher baseline glucagon values (209 +/- 30 pg/ml) than normals (127 +/- 6 pg/ml) and ulcer patients (138 +/- 11 pg/ml) and maintained a higher hormone output throughout the experiment. Together with data on the patient with excluded antral parts it is concluded that the hypercalcemic effect of secretin is not mediated by calcium-regulating hormones but must be of an unspecific nature.
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PMID:Studies on the calcemic effect of intravenous secretin in humans. 122 May 13

Hyperparathyroidism has been associated with an increased incidence of duodenal ulcer, increased acid secretion, and increased plasma gastrin levels. A relationship between these changes, increased serum calcium levels, and the increased incidence of peptic ulceration has been suggested, especially since increased plasma gastrin levels, serum calcium levels, and gastric acid secretion decrease after parathyroidectomy. We have previously suggested that the decrease in plasma gastrin levels after parathyroidectomy may suggest an extragastric source of gastrin, whereas others using immunofluorescent studies have suggested that the parathyroid adenomas themselves might be the source of this gastrin. We prospectively studied in fifteen patients with primary hyperparathyroidism, plasma gastrin and serum calcium levels before and after parathyroidectomy, as well as the gastrin content of parathyroid tumor tissue. The mean basal plasma gastrin level before operation was significantly greater than that of a control group and decreased insignificantly after operation, in contrast to serum calcium levels. No positive correlation could be found between plasma gastrin and serum calcium levels before and after operation. Parathyroid tumor tissue was assayed for gastrin content by radioimmunoassay and no detectable amounts of gastrin could be recovered from any tumor. The results do not support the concept that the extragastric source of gastrin in patients with hyperparathyroidism is the parathyroid adenoma itself.
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PMID:Plasma and parathyroid tumor tissue gastrin and hyperparathyroidism. 124 55

The effect of histamine and betazole hydrochloride (Histalog) on serum calcium homeostasis in the rat was studied in these experiments. Either histamine base, histamine phosphate, betazole, or the appropriate control solution was injected intravenously into fasted, anesthetized 80-100 g male rats. Venous blood was collected before and at 30 and 60 min postinjection. Histamine base in doses of 0.5-2.0 mg/rat induced a significant hypocalcemic response 30 min postinjection which returned to baseline by 60 min. Likewise, the administration of 1.375 mg/rat of histamine phosphate (equivalent to 0.5 mg histamine base) also resulted in a significant fall in serum calcium concentration. However, betazole administration, in doses as high as 10 mg/rat, did not lower the serum calcium concentration. In the histamine experiments neither total protein nor hematocrit values differed from control at the time of hypocalcemia. Therefore the changes in serum calcium concentration cannot be explained by hemodilution. These experiments demonstrate that in the rat the administration of histamine results in a hypocalcemic response similar to that previously observed with gastrin.
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PMID:Histamine-induced hypocalcemia in the rat. 125 Jan 53

Previously we reported a homologous radioimmunoassy for rat thyrocalcitonin (TCT) which was sensitive enough (2--3 ng/ml serum) to measure TCT in thyroid venous blood or thyroid gland extracts but could not detect TCT in peripheral blood even after provocative challenge with iv calcium. In the present study chicken antisera to rat TCT were developed which were sufficiently sensitive (120--240 pg/ml serum) to permit initial evaluation of changes in TCT in rat peripheral blood. The following results were observed: (1) Basal serum TCT in young male Holtzman rats was undetectable, being less than 120--240 pg/ml; (2) induction of marked hypercalcemia by iv calcium increased TCT to approximately 1000--3000 pg/ml within 5 min; (3) thyroid cautery increased TCT to approximately 1000 pg/ml in 5--15 min; (4) calcium gavage (12.2 mg Ca/100 g) produced modest hypercalcemia in 30--60 min and increased serum TCT to approximately 500 pg/ml; (5) injection of isoproterenol raised serum TCT detectably; (6) injection of large doses of gastrin or pentagastrin did not produce detectable increases in TCT 5 or 30 min later. The results show that suitable antisera to rat TCT can be developed in chickens and applied to the measurement, by radioimmunoassay, of elevated circulating levels of TCT in the rat.
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PMID:Improvement and initial in vivo application of the radioimmunoassay of rat thyrocalcitonin. 125 Aug 44

Hypergastrinemia occurs in achlorhydric states if the antrum is not diseased, and evidence has been presented that suggests that antral gastritis diminishes gastrin levels in achlorhydric patients. There is a dramatic gastrin response to calcium challenge in patients with pernicious anemia. Only minimal response was observed in patients with atrophic gastritis. Unlike the response observed in the Zollinger-Ellison syndrome, secretin challenge suppresses gastrin in achlorhydric states. These findings add a new dimension to the utility of serum gastrin determinations.
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PMID:Altered serum gastrin levels in achlorhydric states. 125 59

Thyrocalcitonin (TCT) is a 32 amino acid peptide hormone similar, but not identical, in structure from fish to man. Mammals produce the hormone in non-follicular thyroidal "C-cells" which can be identified visually using recently developed immunocytochemical methods. Although TCT exerts effects on the gut and kidney, bone seems to be the primary target tissue. The ability of TCT to restrict calcium fluxes from bone to blood and to inhibit bone resorption explains its utility for treating certain metabolic bone diseases, e.g. Paget's disease. The bone effects also account for the ability of TCT to combat a hypercalcemic challenge. Recent work suggests close relationships and a possible closed-loop feedback system between the gut and thyroid. In animals, gastrin is a potent TCT secretagogue; studies in man indicate that TCT, in turn, can effect gastric acid secretion and intestinal secretion of water and electrolytes. This gastrin-TCT relationship may help control levels of blood calcium during intestinal absorption of calcium following feeding. The ability of gastrin to stimulate TCT release has been applied clinically for the early diagnosis of medullary thyroid carcinoma (MTC), a C-cell tumor. Subclinical or questionable cases of MTC have been identified reliably using a simple, rapid provocative test involving pentagastrin injection and evaluation of blood samples by radioimmunoassay for elevated levels of TCT.
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PMID:Recent advances with thyrocalcitonin. 125 62


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