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 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

Pulmonary blastoma is an infrequent malignant neoplasm, so called because of its resemblance to fetal lung. The original description outlined the components as variable mixtures of epithelial and stromal elements. More recently, a variant displaying almost exclusively epithelial differentiation has been described. We report our findings in a case of pulmonary blastoma with predominance of epithelial cells, forming tubular structures and large morules. The architectural arrangement of the morules was remarkably similar to normal bronchial neuroepithelial bodies. Moreover, their immunohistochemical profiles were also very similar, including the expression of cytokeratins, chromogranin, neuron-specific enolase, synaptophysin, gastrin, calcitonin, bombesin, somatostatin and serotonin.
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PMID:Pulmonary blastoma with neuroendocrine differentiation in cell morules resembling neuroepithelial bodies. 212 6

Pulmonary tumourlets are focal aggregates of neuroendocrine cells that occur in the periphery of the lung and may be associated with chronic inflammation and scarring. Six such lesions were seen in five lungs from a series of 35 pairs of lungs studied at necropsy. All were immunoreactive for neurone-specific enolase, protein gene product 9.5, and a range of neuroendocrine products. Of the peptides found in neuroendocrine cells in normal human lungs, gastrin releasing peptide was present in all tumourlets and calcitonin in all but one; none contained leucineenkephalin. Of a series of peptide and protein hormones not present in the neuroendocrine cells of healthy human lungs, growth hormone was present in all six tumourlets and adrenocorticotrophin in two. Identical patterns of peptide expression were displayed by neuroendocrine cells in the airway associated with the tumourlets in two cases. Such cells were increased in number and abnormally clustered. Aberrant expression of peptides might accompany the morphological changes in the pulmonary neuroendocrine cells seen in diseased lungs, their florid focal proliferation occasionally resulting in the formation of a tumourlet.
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PMID:Appropriate and inappropriate neuroendocrine products in pulmonary tumourlets. 214 55

This paper presents the results of examinations of 19 cosmonauts, 12 of whom made 7-day flights and 7 took part in space flights of 150, 211 or 237 days. In plasma, parathyrin, calcitonin and gastrin concentrations were measured. A complex mosaic of hormonal regulation of bone metabolism reflects multifactorial and flexible patterns of calcium homeostasis, with individual variations included. It is probable that the specific weight of different components of the system maintaining calcium homeostasis varies depending on the exposure time and activity of related regulatory systems.
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PMID:[Hormonal regulation of calcium metabolism after space flights of different duration]. 221 59

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

To study Ca metabolism in critically ill children, we measured ionized Ca (Ca2+), parathyroid hormone (PTH), calcitonin, 25 hydroxycholecalciferol (25[OH] D3), 1-25 dihydroxycholecalciferol (1-25[OH]2D3, and gastrin levels in critically ill children and in healthy controls. Patients were considered hypocalcemic if Ca2+ was less than 1.1 mmol/L. Six (14%) of 45 patients were hypocalcemic. Five hypocalcemic patients were studied and were found to have higher calcitonin levels than normocalcemic patients and healthy controls and higher PTH levels than healthy controls. 25(OH)D3 and 1-25(OH)2D3 were not significantly different in the three groups of patients. Gastrin levels were low in critically ill patients, whether or not they were hypocalcemic. We conclude that hypocalcemia occurs frequently in critically ill children. It is associated with raised levels of calcitonin and PTH. The mechanism for the increase in calcitonin is unknown.
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PMID:Hypocalcemia and hypercalcitoninemia in critically ill children. 222 88

Recent research has disclosed that neurotransmitters and neuropeptides released within the autonomic nervous system exert homeostatic control of nasal secretion. Although cholinergic and adrenergic influences have long been thought to be the predominant mechanisms, the nonadrenergic, noncholinergic responses may have more suitable, longer-lasting effects. Peptides from sensory nerves, such as calcitonin gene related peptide, substance P, and neurokinin A, may participate in axon response-mediated vasodilation and plasma extravasation. Substance P and gastrin releasing peptide may induce glandular secretion. Defensive responses to local mucosal injury may be amplified by axon response, which initiates these vascular and glandular reactions. Cholinergic effects are primarily responsible for mediating parasympathetic reflexes, but vasoactive intestinal peptide may regulate acetylcholine release, augment glandular secretory responses, and have a vasodilatory effect. In the sympathetic nervous system, neuropeptide Y probably functions as a long-acting vasoconstrictor. Integration of sympathetic and parasympathetic influence may regulate the normal nasal cycle, and sensory and parasympathetic defensive reflexes may respond to epithelial and mast cell stimulation. It is possible, then, that the pathophysiology of vasomotor rhinitis involves an exaggeration of these neural influences.
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PMID:Neuropeptides and nasal secretion. 222 24

The distribution and relative frequency of nerves containing immunoreactivity for substance P (SP), vasoactive intestinal polypeptide (VIP), gastrin-releasing polypeptide (GRP), calcitonin gene-related peptide (CGRP), neuropeptide Y (NPY) and menthionine-enkephalin (MENK) were studied by immunohistochemistry in the gastrointestinal tract of the herbivorous Japanese field vole, Microtus montebelli.
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PMID:Immunohistochemical study of peptide-containing nerves in the gastrointestinal tract of the Japanese field vole, Microtus montebelli. 224 May 82

Bone mineral metabolism was studied in 20 male patients, between 8 and 18 years, after surgical treatment for peptic ulcer (ten Billroth 1 and ten Billroth 2 gastrectomies) and in 16 sex- and aged-matched healthy controls. The bone mineral content was statistically reduced only in the Billroth 2 group. Serum 25(OH)D was lower in all patients, but fractional calcium absorption was similar to the control value. This may be due to increases in 1,25(OH)2D and parathyroid activity (particularly in Billroth 2). Serum osteocalcin levels and hydroxyproline excretion were higher than in the controls. A positive linear correlation emerged not only between serum 1,25(OH)2D and PTH levels but also between each of these and serum osteocalcin and urine hydroxyproline. Both PTH and calcitriol were inversely correlated with the bone mineral mass in Billroth 2, confirming a trend observed in Billroth 1. Although calcitonin values were normal, basal gastrin levels were severely impaired in all patients. In response to a mixed meal, increases in gastrin and calcitonin were significantly lower than in the controls. The calcitonin response to intravenous calcium and pentagastrin infusion was not significantly different to the controls. The percentage increase in gastrin and calcitonin responses to oral calcium correlated positively with the reduction in bone mineral content only in the Billroth 2 group, suggesting a reduction in calcitonin release may contribute to gastric surgery osteopenia in these patients.
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PMID:Partial gastrectomy and mineral metabolism: effects on gastrin-calcitonin release. 226 47


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