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 AA., on the basis of their recent studies, offer a new hypothesis on the role of calcitonin, as a regulator of phosphorus metabolism. In addition the AA. confirm the clear interrelationship between calcitonin and other hormones as gastrin and autonomous nervous system.
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PMID:[Hypersecretion of calcitonin in hypocalcemic syndromes and in stimulation of the autonomic nervous system]. 91 35

Variables of calcium metabolism were measured in 11 patients with clearly documented acute pancreatitis. Total and ionized calcium levels were either low or in the low-normal range as were phosphorus and total magnesium levels. Parathyroid hormone levels were high, and there was a significant inverse correlation with ionized calcium. Gastrin levels were normal, calcitonin values were uniformly below the detection limit of the assay, and pancreatic glucagon levels were elevated. The hypocalcemia of acute pancreatitis was probably not caused by abnormalities of glucagon, calcitonin, or gastrin secretion. Furthermore, parathyroid hormone secretion was apparently not impaired. Hypomagnesemia possibly played a minor role. This study suggests that the hypocalcemia of acute pancreatitis is secondary to extraskeletal calcium sequestration or an as yet unidentified defect of bone metabolism, or both.
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PMID:The hypocalcemia of acute pancreatitis. 114 52

In antrectomized (B-I) and control rats, bone mineralization, the fractional intestinal absorption of calcium, magnesium and phosphorus, the balances of these minerals, their serum concentration and renal excretion, together with serum gastrin, calciotropic hormones (parathyroid hormone, calcitonin, 1,25-dihydroxyvitamin D), and osteocalcin were assessed four months after surgery. B-I evoked hypogastrinemia, but no changes in the serum concentrations of minerals and calciotropic hormones, or urinary cyclic AMP. The major significant changes brought about by B-I were: (1) a decrease in bone dry weight, specific density, bone ash calcium and magnesium content; (2) a decrease in the fractional absorption and urinary excretion of calcium and magnesium; (3) an increase in urinary hydroxyproline and serum osteocalcin in the presence of normal serum bone isoenzyme of alkaline phosphatase. It is concluded that in the rat (1) B-I over the long term decreases both bone mineral content and calcium and magnesium absorption, in the absence of any counterregulation; (2) B-I rats may have attained a new equilibrium which is characterized by decreased absorption and urinary excretion of calcium and magnesium, but maintenance of normocalcemia at the expense of bone; (3) the concomitant changes of serum bone markers are contradictory, which makes their interpretation and use in the present context difficult.
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PMID:Disturbances of mineral and bone metabolism following gastric antrectomy in the rat. 133 20

The effect of calcitonin on gastric emptying of a radiolabelled test meal was examined in 8 male patients with active gastric ulcer. The patients ate the test meal twice, whilst during one of the examinations they were given synthetic salmon calcitonin (415 pmol i.v. bolus + continuous infusion during 90 min to reach an overall dose of 62.25 pmol.kg-1 body mass) and during the other one they received placebo--in randomized order, according to a double-blind study protocol. In every patient a pronounced delay in gastric emptying after calcitonin was observed --the emptying index, Ix: 2.33 +/- 0.22 x 10(-2) min-1 (placebo) vs 0.81 +/- 0.18 x 10(-2) min-1 (calcitonin), p less than 0.001. Calcitonin delayed and significantly lowered the postprandial gastrin release, as well as suppressed the postprandial insulin release with a secondary change in the serum glucose concentration pattern, whereas the serum calcium and phosphorus remained unaffected. The authors conclude that salmon calcitonin in a pharmacological dose elicits a strong inhibitory effect on gastric emptying in gastric ulcer patients.
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PMID:[Effect of calcitonin on gastric emptying after isotope-labeled solid meal in patients with stomach ulcer]. 209 24

The effect of calcitonin on gastric emptying of a radiolabelled test meal was examined in 10 patients with an endoscopically confirmed duodenal bulb ulcer. According to a double-blind study protocol, the patients were given on two different days placebo or synthetic salmon calcitonin (415 pmol i.v. bolus followed by a 90-min infusion to reach an overall dose of 62.25 pmol.kg-1 body mass)--in randomized order. Calcitonin did not affect the postprandial gastrin release nor did it change significantly the serum calcium or phosphorus concentration. The abolished postprandial insulin release by calcitonin was accompanied by a different pattern of serum glucose concentration, when compared to the situation with placebo. In all patients examined calcitonin evoked a profound delay in gastric emptying--the mean gastric transit time, MTT90: 34.1 +/- 1.4 min (placebo) vs 41.0 +/- 1.1 min (calcitonin), p less than 0.001.
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PMID:[Effect of calcitonin on gastric emptying and postprandial secretion of gastrin and insulin in patients with duodenal ulcer]. 209 41

In a double-blind placebo-controlled study, the effect of calcitonin on gastric emptying and on serum concentrations of gastrin, insulin, glucose, calcium and phosphorus after a mixed solid-liquid meal was examined in six patients with type I gastric ulcer. Synthetic salmon calcitonin 415 pmol i.v. was given as a bolus followed by a 90-min infusion to reach an overall dose of 62.25 pmol.kg-1. Gastric emptying of a radiolabelled meal was measured with a gamma camera. Calcitonin suppressed gastric emptying in all patients examined. The mean gastric transit time, MTT90, increased from 38.1 +/- 0.4 min after placebo to 43.1 +/- 0.6 min after calcitonin (P less than 0.001). Calcitonin significantly blunted the postprandial gastrin release: AUC0-90 10,398 +/- 2886 ng. l-1 min (placebo) and 8238 +/- 2573 ng. l-1 min (calcitonin), P less than 0.05, and abolished the postprandial insulin release--AUC0-90 2244 +/- 230 mU.l-1 min (placebo) vs. 638 +/- 198 mU.l-1 min (calcitonin), P less than 0.01. A steady increase in the serum glucose during calcitonin infusion, reaching up to 5.6 +/- 0.31 mmol.l-1 at the end of the infusion, was observed. Calcitonin did not significantly affect serum calcium or phosphorus concentrations. The authors conclude that a delayed gastric emptying is to be expected in patients undergoing calcitonin treatment.
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PMID:Effect of calcitonin on gastric emptying and on postprandial gastrin and insulin release in patients with type I gastric ulcer. 221 26

In a double-blind placebo-controlled study, we examined the effect of calcitonin on gastric emptying, and on serum concentrations of gastrin, insulin, glucose, calcium, and phosphorus after a mixed solid-liquid meal in 11 healthy men. Synthetic salmon calcitonin was administered as a 415 pmol i.v. bolus injection followed by a 90-min infusion to reach an overall dose of 62.25 pmol/kg body mass. Gastric emptying of a radiolabeled meal was surveyed by means of a gamma camera. A pronounced inhibition of gastric emptying with calcitonin was observed in all subjects (median gastric half emptying time 60.3 min after placebo versus 197.6 min after calcitonin; p less than 0.001). Calcitonin did not effect the postprandial gastrin release, nor did it change significantly the serum calcium or phosphorus concentrations. A decreased postprandial insulin release by calcitonin (mean +/- SEM area under the insulin curve 2,124.6 +/- 382.0 min mU L-1 after placebo versus 640.9 +/- 124.0 min mU L-1 after calcitonin; p less than 0.002) was accompanied by a different pattern of serum glucose concentrations during the infusion of the hormone when compared to the situation with a placebo. We discuss potential mechanisms and clinical relevance of our findings.
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PMID:Effect of calcitonin on gastric emptying and on serum insulin and gastrin concentrations after ingestion of a mixed solid-liquid meal in humans. 240 30

In a double-blind placebo-controlled study the effect of glucagon on gastric emptying, as well as on serum concentrations of gastrin, insulin, glucose, calcium, and phosphorus after ingestion of a mixed solid-liquid meal was examined in nine normal males. An i.v. bolus of 0.5 mg of crystalline glucagon was followed by 1.5 mg infused at a constant rate over 90 minutes. The gastric emptying of a radiolabelled meal was measured with the use of a gamma camera. Glucagon evoked a marked delay in gastric emptying in all patients studied--the emptying index, Ix: 2.065 +/- 0.211 min-1 after placebo vs 0.358 +/- 0.090 min-1 after glucagon, p less than 0.01. The postprandial gastrin release was suppressed during the first 60 minutes of glucagon infusion and occurrence of the postprandial increment in the serum gastrin concentration was delayed. The integrated gastrin response did not, however, significantly change: the area under the gastrin curve, AUC0-90, 8733 +/- 1502 min.ng.l-1 after placebo vs 7434 +/- 1372 min.ng.l-1 after glucagon. A promotion of insulin release by glucagon was reflected by a significant increase in the area under the insulin curve, AUC0-90: 1842 +/- 153 min.mU.l-1 after placebo vs 3388 +/- 567 min.mU.l-1 after glucagon, p less than 0.02. Moreover, a sooner and significantly higher increase of the serum glucose level was observed during glucagon infusion when compared to the placebo situation. Glucagon did not significantly change the serum calcium level, whereas the serum phosphorus concentration was markedly lowered throughout glucagon infusion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of glucagon on gastric emptying and on postprandial gastrin and insulin release in man. 248 72

The effect of somatostatin-14 on gastric emptying, as well as on serum concentrations of gastrin, insulin, glucose, calcium, and phosphorus after ingestion of a mixed solid-liquid meal was examined in seven healthy men in a double-blind placebo-controlled study. An i.v. bolus injection of 61 nmol somatostatin was followed by 244 nmol infused at a constant rate over 90 minutes. Gastric emptying of a radiolabelled meal was surveyed with the use of a gamma camera. A weak delaying effect of somatostatin on gastric emptying of a solid meal did not prove to be statistically significant. Somatostatin decreased significantly the postprandial gastrin release: the area under the gastrin curve, AUC0-90, 9954 +/- 2287 ng.l-1 min (placebo) vs 5327 +/- 718 ng.l-1 min (somatostatin), p less than 0.05. At the same time suppression of the postprandial insulin release by somatostatin was observed--area under the insulin curve, AUC0-90, 1450 +/- 161 mU.l-1 min (placebo) vs 501 +/- 60 mU.l-1 min (somatostatin), p less than 0.002. The postprandial increase in serum glucose concentration was initially attenuated, and shifted towards the end of somatostatin infusion, when referred to the placebo situation. Somatostatin did not change significantly the serum calcium or phosphorus concentrations. The results obtained indicate that somatostatin's effect on gastric evacuation is less pronounced in contrast to the significant inhibitory influence of somatostatin on release of gastrointestinal hormones.
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PMID:Effect of somatostatin-14 on gastric emptying and on gastrin and insulin release after ingestion of a mixed solid-liquid meal in man. 257 74

In a double blind placebo controlled study the effect of calcitonin on gastric emptying and on serum concentrations of gastrin, insulin, glucose, calcium and phosphorus after a mixed solid-liquid meal was examined in eight patients with duodenal ulcer. Synthetic salmon calcitonin 415 pmol iv was given as a bolus followed by a 90 minute infusion to reach an overall dose of 62.25 pmol/kg. Gastric emptying of a radiolabelled meal was measured with a gamma camera. Calcitonin markedly delayed gastric emptying in all patients examined. The emptying index (Ix) decreased from 2.979 (0.397)/min after placebo to 0.896 (0.317)/min after calcitonin (p less than 0.001). Calcitonin did not affect significantly postprandial gastrin release: AUC0-90, 8768 (880) pg/l min (placebo) and 7807 (619) pg/l min (calcitonin). Postprandial insulin release was abolished by calcitonin -Auc0-90, 2258 (242) mU/l min (placebo) v 736 (131) mU/l min (calcitonin), p less than 0.001. Parallel to the suppression of insulin release was a steady increase in the serum glucose during calcitonin infusion, with the highest glucose concentration of 5.8 (0.53) mmol/l at the end of infusion of the hormone. Calcitonin did not change significantly serum calcium or phosphorus concentrations. A combination of a delaying effect on gastric emptying with the inhibition of gastric acid secretion elicited by calcitonin warrants further studies of calcinonin in the treatment of duodenal ulcer.
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PMID:Effect of calcitonin on gastric emptying in patients with an active duodenal ulcer. 265 71


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