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)

Growth hormone release-inhibiting hormone (somatostatin), a hypothalamic peptide that inhibits the release of growth hormone and also the secretion of insulin glucagon, and gastrin, was found in the rat stomach and pancreas in a concentration similar to that in the hypothalamus, as measured by radioimmunoassay. Somatostatin was also found in the duodenum and jejunum, but in a smaller concentration. Gel filtration of the extracts of the pancreas and stomach on Sephadex G-25 yielded two immunoreactive peaks, one corresponding in each case to the somatostatin tetradecapeptide. The hormone was not detected in other viscera or the ovaries. The results imply that somatostatin may be synthesized in the pancreas and the stomach in addition to the brain, and may be involved in local regulatory mechanisms for pancreatic and gastric secretion as well as secretion of growth hormone.
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PMID:Somatostatin: abundance of immunoreactive hormone in rat stomach and pancreas. 5 79

Immuno-cytochemical methods were used to identify, in light and electron microscopy, the somatostatin-containing cells of the human antral mucosa. By means of immunoperoxidase and immunofluorescence methods sequentially applied on the same section, it was shown that the somatostatin cells are distinct from the gastrin cell population; these two endocrine cell types are often closely related. On ultrathin sections from aldehyde-fixed. Epon-araldite embedded tissues, the site of storage of somatostatin was localized with the peroxidaseantiperoxidase complexes technique, after removal of the resin by means of sodium ethoxide. This procedure represents a new technical approach to the use of electron-cytochemical techniques. The results indicate that somatostatin, a growth hormone release inhibiting factor, is localized in the endocrine granules of the D cells.
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PMID:Immuno-electron-cytochemical localization of the somatostatin cells in the human antral mucosa. 7 94

Adult rats were rendered diabetic by a single iv injection of streptozotocin (70 or 75 mg/kg). In these rats, serum insulin fell to minimal levels during the 48 h following drug treatment, and this was roughly paralleled by a progressive decrease in the ability of the lung to oxidize glucose. The addition of insulin to diabetic rat lung slices in vitro had no restorative effect on the depressed glucose oxidative rate during a 2 h incubation period; however, two daily treatments of the rats with 1 unit of protamine, zinc insulin completely restored lung glucose oxidation rate to normal, without significantly reducing the hyperglycemic state of the rats. An examination of the temporal changes in glucose utilization by the rat lung after acute insulin treatment revealed that the diabetic lung responded directly to serum levels of insulin, whereas the normal lung appeared to be unaffected by serum insulin levels as hihg as 87 ng/ml. The reduced rate of glucose oxidation in the diabetic lung was apparent after perfusion of the lung with glucose-free medium, and was characterized by a significant reduction in Vmax without an alteration in Km. This was attended by a depressed ability of the lung to incorporate [3H]leucine into protein and an increased ability to produce lactate, but hexose monophosphate shunt activity was normal. Specific receptors for insulin have been identified and partially characterized in crude membrane preparations of normal rat lung. The interaction of insulin with these receptors was rapid, reversible, saturable, and was dependent upon time and temperature. The binding of labeled insulin was inhibited by low concentrations of unlabeled insulin and by high concentrations of proinsulin, whereas it was unaffected by the presence of glucagon, gastrin, prolactin, ACTH, or growth hormone in microgram amounts. These observations suggest that insulin regulates the transport and utilization of glucose in the rat lung, and that this tissue contains specific receptors for insulin.
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PMID:Pulmonary insulin responsivitiy: in vivo effects of insulin on the diabetic rat lung and specific insulin binding to lung receptors in normal rats. 14 46

Monolayer tissue culture has been used as a system in which to study aspects of ectopic hormone secretion. Of a series of twenty-four human bronchial carcinomas, nineteen were successfully established in culture and the supernatant medium from each tested for peptide hormones by radioimmunoassay. Six tumours were found to produce adrenocorticotrophin (ACTH), four to release calcitonin (CT) and one to release both of these hormones. No growth hormone or insulin was detected throughout the series. Net in vitro synthesis of both ACTH and CT was demonstrated by recovery of more hormone during culture than was originally contained in the explanted tumour tissue. The production of hormone by four out of six proliferative cultures established, and its persistence through many subculture passages, confirms ectopic hormone production as a stable heritable characteristic of some lung tumours. The ability of hormone-producing bronchial tumour cells to respond to factors known to influence hormone output from normal endocrine cells was tested. ACTH release was stimulated in one tumour by Pitressin and CT in another by gastrin. In addition, the release of CT from the same tumour cell line was shown to be inhibited by the accumulation of high external concentrations of CT as has been reported for normal C-cells.
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PMID:Ectopic hormone production by bronchial carcinomas in culture. 21 32

Bromocriptine was administered to 2 subjects with gastrin-secreting tumors of the pancreas. The absorption of the drug was confirmed by a rise in growth hormone levels but no change in the elevated serum gastrin levels were observed. Bromocriptine does not appear to affect gastrin hypersecretion in the way that it influences the hypersecretion of pituitary hormones.
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PMID:Failure of oral bromocriptine to affect hypergastrinemia in two patients with the Zollinger-Ellison syndrome. 22 52

The renewal of the digestive mucosa is the most efficient process assuming the maintenance of the gastrointestinal barrier. The mucous and absorptive cells, born in the proliferative zone, are migrating to the surface and they extrude duirng meals, living 4 to 6 days. Hyperphagia, pregnancy, lactation and intestinal resection induce a hypertrophic state. Fasting, ageing, germ free status provoke a hypoplasia. The ulcerogenic and antimitotic drugs decrease the proliferative activity. The gastrointestinal cell renewal is controlled by hormonal, vitaminic and nervous agents. Gastrin and growth hormone are the major trophic factors, secretom amd cprtocpsteroids act as antitrophic agents. The vitamins A, D and B12, and the nervous transmittors participate in the feed back control assuming a steady state between proliferation and extrusion. Chalones and immunologic factors are probably the most important but unknown inhibitors. The pathological events concerned with abnormal renewal are peptic ulcer, atrophic gastritis, intestinal villous atrophy and digestive cancer.
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PMID:[Regulation of cell renewal in the gastrointestinal mucosa (author's transl)]. 32 43

The effect of somatostatin, a growth hormone releasing-inhibiting hormone (GH-RIH) on basal and meal-, pentagastrin-, or histamine-stimulated gastric acid and pepsin secretion was studied in six duodenal ulcer patients. Intravenous GH-RIH infused in graded doses ranging from 0.62 to 5.0 microgram/kg/hr produced a dose-related inhibition of pentagastrin-induced acid secretion reaching about 15% of control level at the dose of 5.0 microgram/kg/hr. Acid inhibition was paralleled by a decrease in the pepsin output and accompanied by a dose-dependent reduction in serum growth hormone and insulin levels measured by radioimmunoassay. GH-RIH used in a single dose of 2.5 microgram/kg/hr produced about 85% inhibition of acid secretion induced by a meal (measured by intragastric titration) accompanied by a significant decrease in serum gastrin and insulin levels. The effect of GH-RIH on histamine-stimulated secretion was very modest and observed only after stopping the GH-RIH infusion. Thus GH-RIH suppressed acid and pepsin secretion induced by pentagastrin and a meal, and this effect was accompanied by a suppression of serum growth hormone and gastrin levels which may contribute to the inhibition of gastric secretion observed.
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PMID:Effect of somatostatin on meal-induced gastric secretion in duodenal ulcer patients. 33 84

Somatostatin, under physiological conditions, is a regulator of thyroid stimulating hormone, growth hormone, pancreatic islet-cell hormones and gastrin. In pharmacological dosage, gastric acid output, splanchnic blood flow and plasma renin levels, are influenced. A possible therapeutic effect on increased growth hormone secretion, disturbances of carbohydrate metabolism, gastroenteropathies and renal hypertension, is discussed. The clinical application is limited by the short biological half-life of the substance and the unspecific action on several organs.
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PMID:[Somatostatin]. 37 88

The serum gastrin response to whole beef extract was measured in 14 duodenal ulcer patients before and after sulpiride administration. A significant inhibition of response was found both after acute intramuscular injection of the drug and after oral administration for 1 week. Fasting serum gastrin was also significantly reduced after chronic treatment; gastric acid secretion did not change. Although the mechanism of the gastrin-lowering action of sulpiride is unknown, it could be mediated by some known effects(s) of the drug, such as modifications in brain monoamine metabolism or perhaps reduced growth hormone secretion.
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PMID:Inhibition of gastrin secretion by sulpiride treatment in duodenal ulcer patients. 56 26

The concentrations of testosterone, cortisone, gastrin, insulin, gastric inhibitory polypeptide (GIP), somatomedin B, parathyroid hormone (PTH), human growth hormone (HGH) and thyroid stimulating hormone (TSH) have been determined in the plasma and the ultrafiltrate of five uremic patients undergoing intermittent hemofiltration treatment. There was a considerable loss of gastrin, insulin, GIP, somatomedin B and PTH by hemofiltration treatment. The plasma concentrations, however, did not decrease except for immunoreactive-PTH (IR-PTH) which returned from elevated to normal levels. Cortisone, HGH and TSH concentrations in the ultrafiltrate were below the measureable range. A significant elimination of 11-hydroxylated androstans by hemofiltration may have a positive effect on the disturbed steroid metabolism. Results indicate that hemofiltration does not cause a hormone deficiency syndrome. On the contrary, the loss of degradation products of hormones with disturbing biological activity may be a favorable effect of the hemofiltration treatment.
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PMID:Assessment of hormone loss through hemofiltration. 68 65


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