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)

The isolated rat liver perfused for 12 hours at pH 7.10 with a suspension of bovine erythrocytes in Krebs-Ringer bicarbonate buffer containing 3 per cent bovine serum albumin has been used as a test system to study effects of glucagon and of dexamethasone in the presence and absence of insulin on net biosynthesis of rat serum albumin, fibrinogen, alpah1-acid glycoprotein, alpha2-(acute phase) globulin, and haptoglobin. Quantitative measurement of perfusate glucose, amino acid nitrogen, and urea affords a basis for determining net glucose and nitrogen balance in the perfusion system. Although the dose of dexamethasone (total 1.0 mug.) used was insufficient to induce synthesis of alpha2-acute phase globulin, net syntheses of albumin, fibrogen, alpha1-acid glycoprotein, and haptoglobin were increased. Glucagon given with dexamethasone depressed albumin and haptoglobin synthesis markedly, but not that of fibrinogen and alpha1-acid glycoprotein. Glucagon with dexamethasone markedly enhanced ureogenesis and glycogenolysis and elicited an exaggerated negative nitrogen balance. The unfavorable effects of glucagon on albumin and haptoglobin synthesis and on nitrogen balance were reversed by giving insulin simultaneously. It is emphasized that insulin is essential for positive nitrogen balance.
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PMID:Direct effects of glucagon on protein and amino acid metabolism in the isolated perfused rat liver. Interactions with insulin and dexamethasone in net synthesis of albumin and acute-phase proteins. 6 Nov 40

Autoantibodies reacting with discrete populations of cells in normal human pancreatic islets were found by immunofluorescence in 17 out of 1279 sera. A double immunofluorescence technique, with antisera to pancreatic glucagon, insulin, somatostatin, and human pancreatic polypeptide was used to show that 13 of the sera contained anitbodies reacting specifically with glucagon cells, while the other 4 reacted with somatostatin cells. These antibodies were directed against intracellular components and not against the hormones themselves. Both types of antibody occurred independently of the islet-cell antibodies which have been described in diabetes mellitus. These findings suggest selective damage to individual cell types in the pancreatic islets and raise the possibility of corresponding hormone deficiency syndromes.
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PMID:Separate autoantibodies to human pancreatic glucagon and somatostatin cells. 6 13

Hepatic encephalopathy (H.E.) is associated with and perhaps caused by changes in plasma-aminoacid patterns--decreased branched-chain aminoacids (B.C.A.A.) and increased aromatic aminoacids (A.A.A.). The decreased B.C.A.A. may be in part secondary to hyperinsulinaemia, but the B.C.A.A. are catabolised by both fat and muscle. The increase in A.A.A. may reflect a "catabolic stimulus" reflected in hyperglucagonaemia, particularly in severe hepatic failure and H.E., and a decreased insulin/glucagon ratio. Endogenous protein, lean body-mass, or liver then releases large amounts of A.A. and the A.A.A. cannot be catabolised by the failing liver, and thus accumulate in the circulation. With decreased plasma-B.C.A.A., the molar ratio of B.C.A.A. and A.A.A. decreases allowing the toxic A.A.A. to penetrate the blood-brain barrier in increased amounts and encephalopathy develops. Appropriate therapy for H.E. must include reversal of the "catabolic state" by providing sufficient B.C.A.A. and calories to decrease the flux of A.A.A. from muscle and liver, and the restoration of the normal molar ratio of B.C.A.A. and A.A.A.
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PMID:Insulin, glucagon, aminoacid imbalance, and hepatic encephalopathy. 6 15

Infusion of somatostatin, an inhibitor of glucagon secretion, in insulin-dependent diabetics resulted in a 75-100% reduction in the blood-glucose rise after oral glucose administration, but did not improve intravenous glucose tolerance. Somatostatin reduced blood-xylose levels by 50-90% after ingestion of this pentose and delayed the peak increment in blood-xylose by 1-2 h. Similar effects on blood-xylose levels and a 30% reduction in splanchnic blood-flow were observed in normal subjects during infusion of somatostatin. Glucagon administration (3 ng per kg per min) or intraduodenal administration of xylose did not reverse somatostatin's effect on xylose tolerance. Somatostatin reduces postprandial hyperglycaemia in diabetes primarily by decreasing and/or delaying carbohydrate absorption rather than enhancing carbohydrate disposal. This effect may be mediated, in part, but a reduction in splanchnic blood-flow. These findings indicate that postprandial hyperglycaemia in diabetes is due primarily to insulin deficiency rather than glucagon excess.
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PMID:Influence of somatostatin on carbohydrate disposal and absorption in diabetes mellitus. 6 40

Extracts of homogenates of rat, mouse, rabbit, and human submaxillary salivary glands contain a significant quantity of a material with glucagon-like immunoreactivity. Fractionation of this material on columns of Sephadex G-100 reveals a single peak immediately following a gamma globulin marker but in advance of a rat growth hormone marker, crystalline amylase, and isotopically labeled porcine insulin and glucagon. This material, which is urea stable, shows identical immunoassay dilution curves when measured with the highly specific K-30 glucagon antiserum. Study of paired glands in vitro shows that low concentrations of glucose stimulate and high concentrations of glucose suppress release of this material. Arginine promotes brisk release in vitro. Somatostatin does not influence arginine-stimulated secretion and insignificantly suppresses basal release in vitro. These findings lend support to previous speculations that the salivary glands may possess endocrine as well as exocrine functions. Salivary gland glucagon may also be the source of circulating glucagon recently reported in pancreatectomized and eviscerated rats.
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PMID:Salivary gland hyperglycemic factor: an extrapancreatic source of glucagon-like material. 6 92

The first case of a tumour producing somatostatin-like immunoreactivity and bioactivity is presented. The pancreatic tumour was composed of cells indistinguishable from islet D cells. Radioimmunoassay of blood-samples obtained by tumour-vein catheterisation revealed very high levels of somatostatin immunoreactivity. On gel chromatography tumour extracts were found to contain at least 4 different immunoreactive components, one of which eluted in the position of synthetic somatostatin. Extracts from the tumour were potent in inhibiting insulin and glucagon secretion from isolated perfused porcine pancreas. Clinical abnormalities included hypochlorhydria, steatorrhoea, and diabetic glucose tolerance. Conceivably some of these abnormalities may be related to somatostatin hypersecretion from the pancreatic tumour.
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PMID:Pancreatic somatostatinoma. Clinical features and physiological implications. 6 72

Whole pancreases from fetal rats of 13 days and 18 days gestation were explanted onto rayon grids and grown in organ culture. Cultures were fixed in Bouin's fluid, sectioned and stained with the fluorescent antibody techniques for glucagon and insulin, aldehyde fuchsin for B cells, pseudoisocyanin for D cells and a silver technique for the fourth cell type. The 13-day explants were fixed after 10 days in culture. A, B and D and the fourth cell type were seen, indicating that precursors of all four endocrine cell types must be present in the fetal pancreas shortly after the formation of the pancreatic bud (11 days). Further, the presence of these four cell types in the walls of tubules in these cultures indicates the tubules as the site of origin of all the endocrine tissue. The 18-day explants were collected every other day of culture from 2 to 30 days in a long-term experiment. A number of large islets with well granulated B cells was still present after 30 days of culture. The relative abundance of cell types at different stages was estimated as follows: 18-day fetal controls, A greater than B=4 greater than D; after 2 to 10 days in culture, B greater than A greater than or equal to D; after 18 to 30 days in culture, B greater than D greater than A greater than 4.
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PMID:A, B, D cells and a fourth cell type in long-term cultures of fetal rat pancreas. 6 78

Implants of rabbit neonatal pancreas, encased in 'Nucleopore' chambers (0.4 micrometer) reversed streptozotocin-induced diabetes in the rat. Blood-glucose, plasma-insulin, and oral glucose-tolerance test returned to normal. An isolated, perfused, streptozotocin-treated pancreas removed from a diabetic animal did not secrete insulin and removal of implants after 6 weeks from six animals caused all animals to die in hyperglycaemia within 8 days. This shows that the implant did not lead to the re-establishment of endogenous pancreatic function. Implanted diced neonatal pancreas in three chambers removed after 6 weeks secreted glucagon, insulin, and pancreatic polypeptide in vitro. No rejection reactions were seen. Rabbit neonatal pancreatic implants may thus be feasible therapy in insulin-requiring diabetic patients. Implants of other non-syngeneic endocrine cells--i.e., pituitary, thyroid, and ovary--may be useful in other hypoendocrine syndromes.
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PMID:Reversal of streptozotocin-induced diabetes in rats by intraperitoneal implantation of encapsulated neonatal rabbit pancreatic tissue. 7 54

Primary cultures of rat liver parenchymal cells maintained as a monolayer in serum-free culture medium were used to investigate the characteristics of zinc accumulation in vitro. Liver parenchymal cells accumulated zinc by a temperature-dependent, saturable process that was inhibited by cyanide, azide, oligomycin, N-ethylmaleimide and iodoacetamide. Cadmium reversibly inhibited zinc accumulation in both serum-free and serum-containing media. Gel filtration chromatographic studies showed that recently accumulated intracellular zinc was present as a low molecular weight complex smaller than metallothionein, the zinc storage protein, but larger than individual amino acids. The quantity of zinc accumulated was affected by preincubation of the cells with various hor?ONES. Dexamethasone, prednisone and prednisolone each increased zinc uptake by 40--50% when either insulin or glucagon was also present. Hydrocortisone, cortisone and sex steroids did not influence zinc accumulation. Removal of the polypeptide hormones from the medium abolished the stimulatory effect of the synthetic glucocorticoid steroid hormones on zinc accumulation.
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PMID:Zinc uptake by isolated rat liver parenchymal cells. 7 27

Pancreatic islet-cell antibodies (ICA) are important markers for two subtypes of insulin-dependent diabetes mellitus and stain the entire islet in the standard immunofluorescence test. This could indicate either a mixture of antibodies each directed against one cell type, or a population of antibodies reacting with a single antigen common to the endocrine pancreas. In the present experiments such a common antigen was demonstrated visually by application of animal antisera raised to each of the 4 pancreatic hormones, together with ICA-positive sera in a four-layer double immunofluorescent technique employing green and red anti-Ig conjugates. Double exposure photographs demonstrated that the patients' sera reacted equally with the different endocrine cells. The ICA antigen did not cross-react with gastric glucagon- or somatostatin-cells. By contrast, human antibodies against glucagon-cells (GCA) or somatostatin-cells (SCA) reacted with discrete antigens specific to each cell type and in 50% of cases the antibodies also stained the respective endocrine cells in the gastrointestinal tract. These refined discriminatory properties of human autoantibodies may lead to a better understanding of the intracellular membrane systems in these important endocrine organs.
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PMID:Islet-cell antibodies (ICA) in diabetes mellitus (evidence of an autoantigen common to all cells in the islet of Langerhans). 8 9


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