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)

Gliquidone (a second generation sulphonylurea) was administered orally to normal rats 1 h before killing. Gliquidone treatment led to a decrease in plasma glucose, an increase in insulin and a diminution in glucagon concentration. Insulin binding to liver plasma membranes was enhanced by 40% in comparison with controls, whereas glucagon binding was slightly diminished. These findings indicate a greater sensitivity of liver cells to insulin during sulphonylurea treatment and support the view that sulphonylureas potentiate insulin action on the liver.
Eur J Clin Invest 1979 Dec
PMID:Extrapancreatic action of sulphonylureas: effect of gliquidone on insulin and glucagon binding to rat liver plasma membranes. 11 39

Using the sensitive protein A-gold technique for the demonstration of antigenic sites in thin section for electron microscopy it was found that in the alpha granules of human pancreas, glucagon immunoreactivity (specific, C-terminal) is restricted to the dense granule core while glicentin immunoreactivity predominates on the peripheral halo surrounding the dense core.
C R Seances Acad Sci D 1979 Dec 10
PMID:[Immunocytochemical anatomy of alpha granules in the human endocrine pancreas]. 12 Dec 70

Everted intestinal rings from partially starved rats accumulate the nonmetabolized amino acid 1-amino-cyclopentane-5-carboxylic acid (ACPC) at an enhanced rate. Plasma glucagon concentrations were found to be markedly elevated in these partially starved rats as well as in rats with experimentally induced diabetes, a condition previously shown to be associated with augmented intestinal uptake of amino acid. Treatment of partially starved rats with repeated injections of glucagon-binding antiserum prevented increased ACPC uptake of intestinal rings. Chronically elevated plasma glucagon levels may participate in the mechanism of the functional changes in the intestine in partial starvation.
Gastroenterology 1975 Dec
PMID:Treatment with glucagon-binding antibodies alters the intestinal response to starvation in the rat. 12 36

Insulin-, glucagon-, and somatostatin-containing cells were evaluated by morphometry in sections of pancreas treated for immunofluorescence. Glucagon- and somatostatin-containing cells were found to be increased in islets of streptozotocin-diabetic rats as compared to control islets.
C R Acad Hebd Seances Acad Sci D 1975 Dec 15
PMID:[Activity of somatostatin-containing cells of the Ilets of Langerhans in experimental diabetes]. 13 Sep 91

D-glucose in the pyranose (ring) form exists as two anomers. The alpha-anomer is more effective than the beta-anomer in promoting insulin secretion, suppressing that of glucagon, and protecting beta-cells against alloxan toxicity. Streptozotocin (SZ), a beta cell toxin, is composed of a cytotoxic moiety, 1-methyl 1-nitrosourea, attached to carbon-2 of glucose and exists as either of two anomers in the pyranose form. In 24-hour-fasted male rats, predominantly alpha- or predominantly beta-SZ was injected intravenously and plasma glucose levels were obtained 48 hours later. The alpha-anomer produced significantly greater beta-cell necrosis at doses of 30, 35, and 40 mg./kg. body weight. At higher doses, no differences between the alpha and beta anomers were observed. 3-O-Methyl glucose (3-OMG) protected against both SZ anomers; however, the alpha-SZ remained more toxic. Larger doses of glucose protected against the lower doses of SZ and, under such conditions, the individual glucose anomers appeared equally potent. Finally, mannitol at comparable molar concentrations was ineffective in protecting against the SZ toxicity. This study suggests that streptozotocin's beta cell toxicity is mediated through recognition by the beta cell. In addition, 3-OMG and, to a lesser but significant extent, glucose were shown to protect against the streptozotocin toxicity, whereas mannitol did not.
Diabetes 1977 Dec
PMID:Pancreatic beta cell toxicity by streptozotocin anomers. 14 86

Twenty-seven patients with symptomatic Paget's disease of bone were randomly treated with mithramycin, glucagon, and calcitonin given either alone or in combination. Mithramycin, at a dose of fifteen micrograms per kilogram of body weight per day, proved to be a relatively safe drug and elicited a rapid response with only transient side effects. Calcitonin combined with mithramycin was the most effective therapy.
J Bone Joint Surg Am 1977 Dec
PMID:Combination drug therapy in treatment of Paget's disease of bone: clinical and metabolic response. 14 41

Heparin was found to be the most potent inhibitor of rat ovarian luteinizing hormone-sensitive adenylate cyclase (I50 = 2 microgram/ml) when compared to other naturally occurring glycosamin oglycans. This inhibition was also apparent when this enzyme was stimulated by follicle-stimulating hormone or prostaglandin E2. Heparin was also found to inhibit glucagon-sensitive rat hepatic adenylate cyclase, and the prostaglandin E1-sensitive enzyme from rat ileum and human platelets. In contrast, heparin stimulated the dopamine sensitive adenylate cyclase from rat caudate nucleus. The sulfated polysugar dextran sulfate exerts similar effects on adenylate cyclase activity of the rat ovary and was shown to inhibit hormone binding to rat ovarian plasma membrane in a manner similar to that exerted by heparin. In contrast to heparin, dextran sulfate inhibited dopamine-sensitive adenylate cyclase from rat caudate nucleus.
Biochim Biophys Acta 1978 Dec 01
PMID:Modulation of adenylate cyclase activity by sulfated glycosaminoglycans. II. Effects of mucopolysaccharides and dextran sulfate on the activity of adenylate cyclase derived from various tissues. 15 57

Elucidation of the role of Ca2+ in the secretion of insulin and glucagon is complicated by the presence of different types of cells in the pancreatic islets. Visualization of calcium in sections of guinea pig pancreas with the histochemical reagent glyoxal bis-2-hydroxyanil revealed the most intense staining in the endocrine part but no differences between various islet cell types. A procedure for eliminating the majority of the beta-cells by streptozotocin injection in the guinea pig enabled a comparison of collagenase-isolated islets rich in alpha 2-cells with islets from untreated animals rich in beta-cells. The latter islets contained 24.6 +/- 2.4 mmol calcium/kg dry wt, as estimated by flameless atomic absorption spectrophotometry. This is twice as much as noted for the exocrine pancreas or the islets rich in alpha 2-cells. After storage for 3 days in culture medium, the two types of islets contained similar amounts of calcium. The cultured islets displayed differences related to cellular composition when measuring the incorporation of 45Ca into a lanthanum-nondisplaceable (intracellular) pool. In the presence of 3 mM glucose, more 45Ca was incorporated into the islets rich in alpha 2-cells. Increasing the glucose concentration to 20 mM with or without further addition of 30 U/liter bovine insulin was without effect on the 45Ca uptake into the islets rich in alpha 2-cells but stimulated that into islets rich in beta-cells. The different calcium dependence on glucose in the two types of islets may indicate that increased uptake of Ca2+ is a component of the mechanism for the secretion of both insulin and glucagon.
Endocrinology 1979 Dec
PMID:Evidence for divergent glucose effects on calcium metabolism in pancreatic beta- and alpha 2-cells. 15 70

1. Hydrocortisone increases in vivo incorporation of [14C] glucose into fetal liver glycogen in the last days of gestation, whereas in glucagon-treated fetuses, a slight decrease in the incorporation rate was found. 2. Hydrocortisone increases total synthetase activity as that of synthetase a but was without effect on fetal liver glycogen phosphorylase. 3. Glucagon causes a slight increase in phosphorylase a activity on days 19-21, and was without effect on the activities of synthetase a and total synthetase. 4. Dibutyryl cyclic AMP had no effect on the key enzymes of glycogen metabolism 1 h after injection in utero, whereas after 6 h an increase in phosphorylase a activity was found without any change in synthetase a activity.
Biochim Biophys Acta 1975 Dec 05
PMID:Effect of hydrocortisone and glucagon on glycogen metabolism in the fetal rat liver. 17 42

Glycogen accumulates in human fetal liver beginning at the eighth week of gestation. A parallel increase in total glycogen synthase activity is found, although the I-form activity remains low and constant throughout the first two thirds of gestation. Total phosphorylase activity increases slightly during this period, with the proportion in the active form amounting to about one half of the total throughout. After an initial rapid decline, the glycogen concentration in explants of human fetal liver remained constant for twenty to forty hours at about 20 per cent of the in vivo level. Incubation with glucagon, cyclic AMP (adenosine 3',5'-monophosphate) or its dibutyryl derivative markedly reduced tissue glycogen concentrations while insulin brought about a small increase. The effect of maximal doses of dibutyryl cyclic AMP and glucagon were the same, and the combination of agents produced no further effect. The response to dibutyryl cyclic AMP was apparent by one hour and maximal by three to six hours, whereas the response to insulin required about six hours to be detected, and it continued for at least eighteen hours. Insulin antagonized the glycogenolytic effect of low doses of glucagon or theophylline but was without significant effect in the presence of high glucagon concentrations. Glucagon stimulated cyclic AMP output from explants, and this effect was further augmented by theophylline. Insultin had no consistent effect on cyclic AMP output in either the presence or the absence of glucagon or theophylline. Incubation with dibutyryl cyclic AMP resulted in a decrease of glycogen synthase I-form activity, while insulin tended to increase this enzyme activity. In neither circumstance was the proportion of active phosphorylase altered. These results suggest that the regulation of glycogen levels in human fetal liver by cyclic AMP, glucagon, and insulin may entail alterations in the activity of glycogen synthase activity without necessitating alterations in phosphorylase activity. Cyclic AMP or glucagon was capable of depleting tissue glycogen stores in tissue from fetuses of six weeks' gestation. Insulin increased tissue glycogen concentrations in tissue from fetuses of seven or more weeks.
Diabetes 1975 Dec
PMID:Hormonal regulation of glycogen metabolism in human fetal liver. I. Normal development and effects of dibutyryl cyclic AMP, glucagon, and insulin in liver explants. 17 97


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