Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent clinical experiences with 34 Z-E patients indicates that the clinical features and course of the syndrome is less dramatic than described originally. Eighty-five per cent of the patients presented stories of abdominal complaints lasting more than five years and resembling the complaints presented by duodenal ulcer patients (DU). Ulcers were present in 91 per cent of the patients. Fifty-one per cent had either ectopic or multiple ulcers. One third had a single duodenal ulcer resembling an ordinary ulcer. No patients died from complications to the ulcer diathesis. Marked hypersecretion of acid and gastrin was present in the ZE group (BAO:33.7 +/- 7.4; PAO:62.8 +/- 6.1 meq H+/h; gastrin: 5094 pmol/l), but because of great individual variation in the ZE, some overlapping with the acid and gastrin measurements of the DU was seen. The diagnostic value of provocative tests using secretin, calcium, glucagon and food stimulations demonstrated a considerable overlapping between the two groups, indicating that these tests are of little clinical value. Tumours were found in half the patients, revealing malignancy in ten. The ZE can be diagnosed in most cases by combining symptomatology, with measurements of acid and gastrin.
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PMID:The clinical diagnosis of the Zollinger-Ellison syndrome. 29 36

Hypergastrinemia and hyperglucagonemia follow portacaval shunt (PCS) or cirrhosis in man and experimental animals. The cause is unknown although portal diversion and hepatic dysfunction are suggested. In these studies transhepatic techniques were used to define the hepatic handling of basal and arginine-stimulated gastrin and glucagon levels in sham-operated and portacaval-shunted pigs and in a group of pair-fed sham-operated pigs. After PCS, basal gastrin levels were lower than those in sham-operated animals but were also lower in the pair-fed group, suggesting that the change resulted from partial starvation. Arginine-stimulation caused a rise in hepatic venous levels in PCS and in pair-fed pigs and in portal venous levels in sham-operated pigs. These data also suggested a response to diminished intake in PCS pigs. There was an immediate transitory rise in portal immunoreactive glucagon (Unger 30K) after PCS and a subsequent rise from the 4th postoperative day in all circulations. Arginine stimulation caused in sham-operated and PCS pigs a biphasic rise in the portal circulation and a later rise in the arterial circulation in PCS pigs. These data suggest that the effect of PCS upon gastrin levels is associated with the impaired appetite while the effect upon glucagon is the result of diversion past the liver.
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PMID:Transhepatic hormone levels in the portacaval shunted pig--the effects of arginine upon gastrin and glucagon release. 29 Feb 69

The stomach of the monkey Tupaia belangeri was investigated by serial sections utilizing the indirect immunoperoxidase reaction to demonstrate the distribution of glucagon, gastrin and somatostatin immunoreactive cells. A striking topographical distribution was found. Glucagon and somatostatin immunoreactive cells were located in the upper parts, whereas gastrin and somatostatin immunoreactive cells were situated in the lower parts of the stomach. The remaining regions of the stomach did not contain cells immunoreactive to the antisera applied. Similarly, the ultrastructural study revealed the same distribution of endocrine cell types identified as A-cells, D-cells, and G-cells. Thus, there may be a glucagon-somatostatin area in the upper part and a gastrin-somatostatin endocrine surface in the lower part of the stomach. This spatial relationship of the endocrine cells suggests a functional cell interaction between glucagon and somatostatin cells in the cranial stomach and between gastrin and somatostatin in the caudal parts of the stomach.
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PMID:Relationship of glucagon-somatostatin and gastrin-somatostatin cells in the stomach of the monkey. 31 3

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

A case with proteinlosing gastropathy with gastric hypersecretion of H+ and pepsin as well as hypergastrinemia is presented. Zollinger-Ellison syndrome was excluded by reduction in acid secretion and serum gastrin during the observation period as well as by the effect on gastric secretion and serum gastrin after injections of secretin and glucagon.
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PMID:Proteinlosing gastropathy with gastric hypersecretion of acid (H+) and pepsin and hypergastrinemia. A case report. 33 48

The neurotensin-cell is identified immunohistochemically and ultrastructurally by differential counting of endocrine cells in the gut of a primate (Tupaia belangeri). Utilizing light microscopy, the EC-cells are identified by the Masson-Fontana silver stain; with the same method the neurotensin cells are not stained. The other endocrine cells have been quantified in the small intestine using the peroxidase-antiperoxidase stain with antisera against glucagon, somatostatin, cholecystokinin, gastrin, secretin, pancreatic polypeptide, gastric inhibitory peptide and neurotensin. In the ileal mucosa of Tupaia, the most frequent endocrine cell is the EC-cell followed by the glucagonoid cell, (L-cell). The immunoreactive neurotensin cell represents the third most frequent endocrine cell in this region. On the ultrastructural level, this third most frequent endocrine cell is a heretofore undescribed cell, the N-cell, containing electron dense secretory granules measuring 335 +/- 87 nm in diameter.
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PMID:Ultrastructural identification of a new cell type--the N-cell as the source of neurotensin in the gut mucosa. 33 60

This is a review of current information concerning the role of hormones and the autonomic nervous system in the control of exocrine secretions of the pancreas. A greater emphasis has been placed on the role of hormones because of information accumulated during the last several years. With the development of radioimmunoassay techniques, it is now possible to correlate circulating hormone concentrations with biological function. The role of hormones has been discussed with the framework of the secretin-glucagon family, the cholecystokinin-gastrin family, and other proposed gastrointestinal hormones and related peptides. Gastrin, secretin and cholecystokinin-pancreozymin are three prime gut hormones that regulate pancreatic secretion. Other hormones that may have a role in pancreatic secretion include glucagon, vasoactive intestinal polypeptide, chymodenin, somatostatin, pancreatic polypeptide, motilin, and bombesin. Neural mechanisms play an important although not so succinct a role in the over-all control of exocrine secretion. A complex relationship exists between the parasympathetic nervous system and the release of the hormones and their effect on pancreatic acinar and duct cells.
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PMID:Neurohormonal control of pancreatic secretion. A review. 34 Mar 22

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


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