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)

We studied the pancreatic and enteric hormone profile of a 46-year-old woman who had hyperglycemia and a pancreatic tumor. Before operation, there was no evidence of overproduction of glucagon or insulin. The tumor's ultrastructure had a distinctive endocrine morphology, resembling D cells. Prompted by the recent demonstration of somatostatin in D cells of pancreatic islets, we analyzed the tumor and found a large quantity of immunoreactive somatostatin (301 ng per milligram of tissue). Insulin, glucagon, gastrin, vasoactive intestinal polypeptide and human pancreatic polypeptide were present in only trace quantities. The tumor cells were cultured in monolayers, which remained viable up to 51 days and released somatostatin into the culture medium. In seven insulinomas and two glucagonomas, we found the somatostatin content either much lower (less than 0.6 ng per milligram of tissue) or undetectable. After complete resection of the tumor, our patient became euglycemic and has remained so for the past 20 months.
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PMID:"Somatostatinoma": a somatostatin-containing tumor of the endocrine pancreas. 32 60

In order to correlate the different cell types of the human endocrine pancreas to a specific secretion product, an immunoelectron microscopic localization of the hormones whose production had been attributed to pancreatic islets was conducted. Glucagon and insulin were respectively localized in the typical A- and B-cells, whereas no subclasses of A-cells could be identified. With antibodies that reacted with the gastrin cells in the human gastric mucosa, it was not possible to detect gastrin in any of the islet cell types. In confirmation of recent results obtained by light microscopy, somatostatin was found in all the typical D-cells containing large, weakly electron-dense secretory granules. The human pancreatic polypeptide (HPP), a newly postulated hormone, was clearly associated with a fourth cell type, which is characterized by the presence of small secretory granules (100-150 nm.). These results suggest that each of the four cell types that are easily identifiable by ultrastructural observations is responsible for the production of a specific secretory product.
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PMID:Identification of four cell types in the human endocrine pancreas by immunoelectron microscopy. 32 32

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

A diagnosis of the heritable disorder Sipple's syndrome was made in a Japanese male aged 28 years. The coexistence of bilateral phenochromocytomas, bilateral medullary thyroid carcinomas and secondary hyperplasia of parathyroid was confirmed at the time of autopsy. Pancreatic islets were hyperplastic with marked proliferation of A and D cells. Transition of the ductal cell to the islet, i.e. "nesidioblatosis" was observed. There was no proliferation of B cells, but a retention of B cell granules, a manifestation of suppressed secretion of insulin attributed to the overproduction of catecholamines was evident. In the stomach, numerous petechial hemorrhages and proliferation of gastrin cells were found. The pathogenesis of changes in the pancreatic islets and stomach is discussed from the viewpoint of hormonal disorders induced by pheochromocytoma and medullary thyroid carcinoma such as are found in Sipple's syndrome.
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PMID:Sipple's syndrome with peculiar changes in pancreatic islets--an autopsy case. 33 54

Somatostatin (cyclic growth-hormone release-inhibiting hormone--GH-RIH) was infused into dogs with gastric fistulae. Somatostatin inhibited gastric acid response to four gastric stimulants--insulin, food, histamine, and pentagastrin. Histamine- and pentagastrin-stimulated pepsins were inhibited similarly to inhibition of acid. Somatostatin inhibited the gastrin response to insulin and food.
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PMID:Inhibition by somatostatin (growth-hormone release-inhibiting hormone, GH-RIH) of gastric acid and pepsin and G-cell release of gastrin. 34 81

Effects of synthetic xenopsin on endocrine pancreas and gastric antrum in anesthetized dogs were studied. Synthetic xenopsin was administered into the superior pancreaticoduodenal artery and plasma insulin, glucagon and gastrin in the superior pancreaticoduodenal vein and gastrin in the right gastroepiploic vein were measured radioimmunologically. Administration of 10 microgram of xenopsin per kg of body weight brought about a hyperglycemic response and rapid and sharp elevations of the hormones in the pancreatic vein. Plasma gastrin level in the gastric vein also showed an immediate and sharp increase following xenopsin administration. Xenopsin appeared more potent inducer of the glucagon. It is concluded that xenopsin acts directly on endocrine pancreas and gastric antrum to secrete their hormones.
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PMID:The effects of xenopsin of endocrine pancreas and gastric antrum in dogs. 35 74

Using indirect immunofluorescence, indirect immunoperoxidase, and unlabelled antibody enzyme techniques, gastrin, pancreatic glucagon, insulin, and somatostatin were localised in sections of both wax- and resin-embedded tissues that had been fixed in a buffered formalin solution. Ultrastructural preservation of the resin-embedded samples was also adequate for combined electron microscopy and light microscope immunochemistry. As the fixative concerned is stable it can be permanently available in surgical units. It is suggested, therefore, that this fixative should prove useful as an alternative to buffered formaldehyde, which must be freshly prepared from paraformaldehyde powder, in institutions where specimen collection is difficult or which have to refer cases with an endocrine involvement to other laboratories for immunochemical and fine structural examination.
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PMID:A formalin fixative for immunochemical and ultrastructural studies on gastrointestinal endocrine cells. 37 49

The effect of an infusion of natural motilin on the rate of gastric emptying of a standard breakfast was studied in 5 subjects using Caesium 129-tagged resin particles. Emptying rates were measured on 4 separate days. On 2 days, the subjects receive only saline (controls), while on the other 2 days a motilin infusion of 0.34 pmol/kg/min for 60 min, followed by 0.68 pmol/kg/min for 60 min, was given. All infusions were blind and given in random order. At the end of the low-dose motilin infusion 31 +/- 4% of the meal had emptied, compared with 17 +/- 2% with saline infusion (P less than 0.01). A similar effect was also seen with the high-dose infusion. Plasma motilin concentrations rose from a basal of 68 +/- 13 pmol/liter to 126 +/- 10 pmol/liter during low-dose motilin infusion and to 170 +/- 11 pmol/liter during the high dose. No significant change in basal or postprandial levels of glucose, gastrin, pancreatic glucagon, pancreatic polypeptide, gastric inhibitory peptide, enteroglucagon, or vasoactive intestinal peptide was noted, but postprandial insulin release was greater during motilin infusion.
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PMID:Effect of motilin on the rate of gastric emptying and gut hormone release during breakfast. 37 76

A 45-year-old man was operated for surgical treatment of a long-standing peptic ulcer disease and upon inspection of the pancreas for suspected Zollinger-Ellison syndrome, tumor nodules were found in this organ. The tumor tissue examined by immunofluorescence showed specific staining only after incubation with anti-pancreatic polypeptide. Negative results were obtained with antisera directed against insulin, pancreatic glucagon, somatostatin, GLI, VIP, secretin, and gastrin. Examination of the tissue by electron microscopy revealed a homogeneous population of small granule-containing cells. This case, therefore, illustrates a tumor composed of one single hormone-producing cell type and allows definition of the ultrastructural features of human pancreatic polypeptide-containing cells.
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PMID:Human islet cell tumor storing pancreatic polypeptide: a light and electron microscopic study. 37 22

To examine gut-islet interrelationships, we entirely separated the gastrointestinal tract from the rat. When we arterially perfused this preparation with an erythrocyte-free solution for 1 h, it remained histologically intact and took up oxygen and glucose. Feedings were given via a duodenal tube. The gut absorbed glucose when glucose in the feeding was high (9.2 g/dl), but not when glucose in the feeding was low (58 mg/dl). With feeding, the portal venous effluent (PVE) from this preparation (stomach to ileum) enhanced late-phase, glucose-induced insulin secretion from pancreas of another rat. This enhancement occurred when the gut was fed either glucose (9.2 g/dl) in electrolyte solution or electrolyte solution alone. PVE from glucose-fed upper gut (stomach, duodenum) was similarly insulinotropic. In contrast, PVE from unfed gut or from glucose-fed gut of old rats was not insulinotropic. PVE from all gut preparations except upper gut produced a glucagon "spike" during basal pancreatic perfusion. Effects of gastrointestinal peptides (gastric inhibitory polypeptide, cholecystokinin octapeptide, secretin, gastrin) and immunoassays of PVE suggested that the insulinotropic substance is not one of these peptides. Thus, an insulinotropic substance that is not dependent on feeding nutrient material is secreted from the intestine.
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PMID:Secretion of an insulinotropic factor from isolated, perfused rat intestine. 37 52


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