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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The proposition that glucagon plays an essential part in maintaining hyperglycaemia in diabetes has been investigated by the study of 5 totally pancreatectomised subjects and 5 age and sex matched insulin-dependent diabetic patients. True basal glucagon values were obtained by the use of a new affinity chromatography technique. The mean fasting plasma-glucose levels of the pancreatectomised subjects was 251 +/- 46 mg/dl. The mean fasting plasma-glucagon level was not significantly elevated above zero (1-3 +/- 0-6 pmol/l) and showed no change following arginine. In the 5 insulin-dependent diabetics the mean fasting plasma-glucagon level of 17-2 +/- 5-3 pmol/l rose to a maximum at 25 minutes of 103-6 +/- 27-5 pmol/l during infusion of arginine. These findings imply the absence of a significant number of normally functioning alpha cells in extrapancreatic sites in man and demonstrate that pronounced hyperglycaemia may occur in the absence of glucagon. Glucagon is probably not of primary importance in the hyperglycaemia of insulin-dependent diabetics.
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PMID:Pancreatectomised man: A model for diabetes without glucagon. 5 31

Diazoxide 5 mg/kg/day was administered to four normal subjects for five days and, together with insulin, to ten diabetic subjects for seven days. In every case there was a substantial increase in the insulin response to combined stimulation of the pancreatic beta cells with 1 mg of glucagon and 2 g of tolbutamide given intravenously. Similar increases were not seen in four diabetics who received placebo with insulin. It is likely that the observed improvements reflected increased insulin stores which resulted from diazoxide inhibition of insulin release. These findings suggest that poor insulin responses in diabetics may be due, at least in part, to chronic overstimulation of the beta cells. Pharmacological agents such as diazoxide, which inhibit glucose-induced insulin release, may have a place in preserving and restoring insulin secretion in diabetes.
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PMID:Improvement in insulin secretion in diabetes after diazoxide. 5 17

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

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

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

An enkephalin analogue [D-Ala2, MePhe4, Met(o)-ol] enkephalin (DAMME), given intravenously to normal subjects raised serum prolactin and growth-hormone levels but lowered serum levels of luteinising hormone, follicle-stimulating hormone, cortisol, and corticotrophin. There was also a small fall in total glucagon and gastric inhibitory peptide (G.I.P.) and a rise in thyrotrophin. beta-Lipotrophin, motilin, vasoactive intestinal peptide, insulin, gastrin, and pancreatic glucagon were unchanged. Blood-glycerol increased, and blood lactate, alanine, and glucose fell. Prior administration of the opiate antagonist, naloxone, attenuated the hormonal responses to DAMME. This enkephalin analogue produces endocrine and metabolic changes in man which may be mediated through opiate-binding receptors both within and outside the brain. The enkephalins and related substances may provide an important link between perception, behaviour, and neuroendocrine regulation of hormone secretion and metabolism.
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PMID:Hormonal and metabolic responses to an enkephalin analogue in normal man. 8 35

Drug-induced porphyrin accumulation occurs in chick embryo liver cells maintained in serum-free Waymouth MD 705/1 medium. Addition of insulin and thyroxine to the medium results in a marked enhancement of porphyrin accumulation. The addition of hydrocortisone results in a further enhancement of porphyrine accumulation. Several agents which are reported to increase intracellular adenosine 3':5'-monophosphate (cAMP) levels, viz. glucagon, sodium fluoride, cAMP or its dibutyryl derivative, 3-isobutyl-1-methylxanthine and papaverine enhanced drug-induced porphyrin biosynthesis. On the other have, agents which are reported to decrease intra-cellular cAMP levels, viz. alloxan and imidazole, diminished drug-induced porphyrin accumulation. cAMP appears to enhance, but not to function as a "second messenger" in drug-induced porphyrin biosynthesis. Drug-induced porphyrin accumulation in chick embryo liver cells depend upon the insulin to glucagon ratio. A low level of porphyrin accumulation occurs at insulin to glucagon ratios similar to those found following glucose administration in vivo, suggesting a possible explanation for the therapeutic effect of glucose in hepatic porphyria. The 5 alpha A(A:B trans) and 5 beta H(A:Bcis) steroids are equipotent in inducing delta-aminolevulinic acid synthetase and porphyrin accumulation in chick embryo liver cells maintained in serum-free culture medium. Thus, there is no specific steric requirement for porphyrin-inducing activity in steroids.
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PMID:Hormonal effects on the regulation of hepatic heme biosynthesis. 8 65

The authors made a comparative study of the use of glucagon (4 mg/day IV) in 30 dogs with acute pancreatitis. They found that the mortality and amylasemia were significantly lower in the glucagon-treated group than in the control groups (saline and glucose solution 5%). In the glucagon group, the areas of necrosis were smaller (1.5 cm) and rarely found; microscopically, the areas of necrosis and the inflammatory reaction were much smaller than in the other groups. These findings lead to the conclusion that the beneficial action of glucagon is due to another mechanism other than its hyperglycemic effect and that the administration of hypertonic solutions of glucose does not have a beneficial effect in acute pancreatitis.
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PMID:[Treatment of acute pancreatitis by glucagon. Experimental studies in dogs]. 9 32


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