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)

A nonfunctioning strumal carcinoid arising in a 49-year-old woman was studied by histochemical and immunocytochemical techniques. All tumor cells, irrespective of their architectural arrangement, showed properties of neuroendocrine-programmed cells, without any evidence of thyroid follicular cell differentiation. Foci of calcitonin-producing C-cells were demonstrable by immunocytochemical technique and were closely associated with areas of amyloid stroma of the tumor. Efforts at localization of insulin and gastrin within the tumor cells gave negative results. While the results in the present case offer additional support for an APUD cell origin of strumal carcinoids, the presence of the calcitonin-producing C-cells within the tumor raises interesting histogenetic possibilities as to whether these lesions are derived from C-cells or represent an ovarian carcinoid with foci of C-cell differentiation.
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PMID:Immunocytochemical localization of calcitonin-producing cells in a strumal carcinoid with amyloid stroma. 37 90

After total gastrectomy and different forms of reconstruction as well as before and after B II-B I conversion, an oral glucose tolerance test was performed in 24 patients, and insulin and gastrin secretion were measured. The results in the patients with preserved or reestablished passage of the glucose through the duodenum demonstrate that (1) the glucose tolerance is significantly better, (2) the secretory capacity of the beta-cells is about twofold greater, and (3) the postprandial gastrin secretion is about threefold greater.
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PMID:[The significance of duodenal passage for insulin and gastrin secretion in patients following total gastrectomy]. 37 83

The distribution of peptide hormone-like immunostaining in the gastrointestinal tract of 11 teleost species was investigated by immunofluorescence. Cells immunoreactive for somatostatin were found in the glandular epithelium of the stomach of four species and in the epithelium of the pyloric appendage of one species. The mid-gut epithelium contained cells reactive with antibodies to glucagon (three species), gastrin (five species), pancreatic polypeptide (five species), and substance P (two species). Cells immunoreactive for met-enkephalin were found in the epithelium of both the mid-gut and the stomach of six species. In six species in which the endocrine pancreas was investigated, insulin-, glucagon-, and somatostatin-like immunoreactivity was observed. Pancreatic polypeptide was definitely localised by immunostaining in cells of the endocrine pancreas of only one out of three species examined. Vasocative intestinal polypeptide-, neurotensin-, bombesin-, and enkephalin-like immunoreactivity was identified in the gastrointestinal nerve fibres in various species. In view of the considerable species variation found, caution should be exercised in generalising about the peptides present in the gastrointestinal tract of fish.
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PMID:Peptide hormone-like immunoreactivity in the gastrointestinal tract and endocrine pancreas of eleven teleost species. 38 3

Fasting gastrinemia in cirrhotics (48.35 +/- 2.77 pg/ml) was higher than in normal controls (32.93 +/- 0.75 pg/ml; P less than 0.001). After insulin-induced hypoglycemia, the mean increase of gastrin above basal level was 42.29 +/- 1.92 pg/ml in controls and 10.85 +/- 5.05 pg/ml in cirrhosis (P less than 0.001). BAO was 2.53 +/- 0.36 mEq/h in controls and 0.42 +/- 0.004 mEq/h in cirrhotics (P less than 0.001). After i.v. insulin, TAO was 8.42 +/- 0.72 mEq/h in controls and 3.06 +/- 0.26 mEq/h in cirrhotics (P less than 0.001). The authors suggest that the lack of an adequate gastrin and acid response to the hypoglycemic stimulus in cirrhotics might be accounted for by a decreased insulin sensitivity.
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PMID:Gastrin response to insulin in patients with cirrhosis of the liver. 38 37

Different types of vagotomy have been widely used in the treatment of peptic ulcer disease. A close relationship between the vagus nerve and the release or action of gastrointestinal hormones is necessary for the optimal activation of the gastrointestinal tract. The serum concentrations of the antral hormone gastrin are elevated after all types of vagotomy. The postvagotomy hypergastrinemia is due to the change in pH in the antral lumen or the gastric motility changes, both of which may lead to a proliferation of G cells. The reduction in pancreatic secretion after vagotomy is not due to changes in intestinal hormone release, but may be caused by the interruption of a postulated enteropancreatic reflex. Postprandial GIP release and serum insulin levels are not affected by vagotomy, but basal GIP levels are increased after vagotomy. Postprandial pancreatic polypeptide release is nearly abolished by vagotomy, but seems to normalize in the later postoperative course. These findings may be important for the interpretation of pathophysiologic changes after vagotomy.
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PMID:Effect of vagotomy on gastrointestinal hormones. 39 Sep

Complementing cytochemical and ultrastructural studies, immunocytochemistry may be used to define, in terms of immunoreactivity, the nature of the polypeptide(s) made and stored in the cells of the endocrine pancreas, islet or otherwise. Immunoserums are applied to histological sections after fixation of the material in Bouin's fluid, and in accordance with four protocols: indirect immunofluorescence, immuno-enzymatic technique, variants in prolonged primary incubation and the method of soluble peroxidase-antiperoxidase complexes. Certain precautions are essential for correct interpretation. In the adult, four essential immunoreactions, corresponding to hormones or "local hormones" are regularly detected:insulin, pancreatic glucagon, somatostatin, pancreatic polypeptide. The cytochemical and ultrastructural characteristics of the cells involved are known (B, A and D cells for the first three specificities). C-peptide immunoreactivity is easily identified, but other immunoreactivities are more irregular or contested: gastrin, cholecystokinin, vasoactive intestinal peptide, ACTH, met-enkephalin.
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PMID:[Practical immunocytochemistry of the endocrine pancreas]. 39 37

Plasma gastrin concentrations and gastric acid output after modified sham feeding were determined in 20 duodenal ulcer patients. Sham feeding produced an acid response corresponding to 40-68% of the maximal acid output after pentagastrin stimulation, with no significant increase of plasma gastrin concentrations. In eight patients proximal gastric vagotomy almost abolished the acid responses to both insulin hypoglycaemia and sham feeding. Sham feeding in the vagotomised patients did not change the gastrin concentrations in plasma. After pretreatment with benzilonium, an anticholinergic with minimal central nervous effects, plasma gastrin concentrations increased after sham feeding. The study confirms that sham feeding is a poor stimulus for gastrin release in duodenal ulcer patients and supports a cholinergic inhibition of gastrin release. Intravenous injection of benzilonium bromide in a dose close to 70 micrograms/kg, and atropine in the low dose of 30 micrograms/kg inhibited the acid response to sham feeding by about 65%. Atropine in a dose of 50 micrograms/kg virtually abolished the acid sham feeding response, possibly owing to ganglionic or central nervous blockade. Vagal activation of the acid secretory glands does not seem to involve a purely cholinergic neurotransmission.
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PMID:Effect of proximal gastric vagotomy and anticholinergics on the acid and gastrin responses to sham feeding in duodenal ulcer patients. 39 71

In 21 female Beagle dogs an experimental pancreatitis was induced by injection of bile into the pancreatic duct system. Beside controls, dogs received 62.5 micrograms/h cyclic somatostatin (SRIF) a continuous i.v. infusion starting with a bolus of 250 micrograms 15 minutes before or 2 hours after bile injection. Following blood parameters were determined: lipase, amylase, blood count, minerals, glucose, insulin, gastrin, secretin and CCK. Two controls died within 24 hours, the others were sacrificed after 48 hours. All pancreata were examined morephologically. The controls developed all clinical signs of acute hemorrhagic pancreatitis, whereas all SRIF-treated dogs were in much better general condition. Lipase and amylase increased in all groups. In the controls insulin, gastrin and secretin remained unchanged and CCK rose slightly. SRIF-treatment diminished insulin, CCK and the test meal-induced increase of secretin. At autopsy the pancreata of the controls were nearly entirely apoplectic. The SRIF-treated dogs showed less damage of the pancreas and no severe hemorrhagic necrosis was noted. The beneficial effect of SRIF cannot only be due to an interaction with intestinal hormones. An additional direct protective effect on the exocrine parenchyma is proposed to exist.
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PMID:Effect of somatostatin on bile-induced acute hemorrhagic pancreatitis in the dog. 39 59

Immunocytochemical techniques, applied to material fixed with Bouin's fluid and using immune sera specific to various hormonal polypeptide(s), give a classification of pancreatic and pancreatico-duodenal apudomas based upon cellular functional activity. With a rane containing a minimum of five antibodies (gastrin, insulin, glucagon, somatostatin and pancreatic polypeptide), 15 tumours could be identified amongst the 22 tested. They were either "monohormonal" tumours (10 cases) or "bi- or polyhormonal" tumours (5 cases). In the remaining 7 cases, only rare cells were immunoreactive. A large number of immunoreactivities thus revealed in histological sections are clinically silent or are present in a "forme fruste".
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PMID:[Immunocytochemistry of pancreatic and pancreatico-duodenal apudomas]. 39 71

The effects of endogenous hypergastrinemia and hypogastrinemia on the exocrine and endocrine pancreas were studied in the rat. Hypergastrinemia was induced by antral exclusion, and hypogastrinemia by antral resection. The studies were made 14 weeks after surgery. The total weight of the pancreas was increased both in hypergastrinemic and hypogastrinemic animals, due to hypertrophy of the exocrine cells. In contrast, the volume and total weight of the pancreatic islets were decreased. There was no numerical difference in the A-, D-, PP-cells between the hyper- and hypogastrinemic animals, respectively, and the controls. The number of insulin-producing (B-) cells was certainly reduced after the induction of hypogastrinemia. There was, however, signs of increased B-cell activity, which might contribute to an underestimation of the number of B-cells with the technique used. These findings do not support the hypothesis that antral gastrin has trophic influence on either exocrine or endocrine pancreas.
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PMID:The effects of endogenous hypergastrinemia and hypogastrinemia on the exocrine and endocrine rat pancreas. 39 7


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