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

The effect of changes in the extracellular redox-state on glucagon-stimulated glucose release by intact isolated rat hepatocytes and the perfused liver was examined. For hepatocytes from the fed rat an increase in pyruvate, ammonium ion or oxygen concentration or a decrease in the lactate/pyruvate or sorbitol/fructose ratios decreased the ability of 1 microM-glucagon to stimulate glucose release without significantly altering the control rate. These changes coincided with a decrease in the lactate/pyruvate ratio of the cell suspension. A decrease in the lactate/pyruvate ratio also decreased the ability of 1 microM-glucagon to stimulate glycogen breakdown measured by loss of contained radioactivity. For the isolated perfused rat liver (fed rat) maximal effects of glucagon as a stimulant of glucose release occurred when lactate instead of pyruvate was present in the perfusion medium. It is concluded that the efficacy of glucagon as a stimulant of glucose release by isolated hepatocytes and the perfused liver depends upon the cytoplasmic redox-state represented by the intracellular lactate/pyruvate ratio.
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PMID:An effect of extracellular redox state on the glucagon-stimulated glucose release by rat hepatocytes and perfused liver. 88 74

Gluconeogenesis was stimulated by glucagon in fed but not fasted isolated perfused guinea pig livers. Both the amount and the rate of incorporation of radioactivity into glucose from L-[U-14C]lactate were increased in fed livers by the addition of glucagon to the perfusate. The glucagon-stimulated increase in gluconeogenesis was accompanied by an increase in oxygen consumption, an increase in the amount of lactate carbon converted to glucose and a decrease in the amount of lactate carbon converted to CO2. The results are interpreted to indicate that glucagon affects gluconeogenesis from lactate in fed livers by redirecting the fate of substrate from other products toward glucose.
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PMID:Gluconeogenesis in the guinea pig. Effect of glucagon on gluconeogenesis from lactate by isolated perfused guinea-pig liver. 89 28

1. Adrenal and pancreatic endocrine responses to hypoxia and hypercapnia, of differing degrees of intensity, have been examined in conscious, unrestrained calves 3-5 weeks after birth. 2. The outputs of cortisol and corticosterone from the right adrenal gland were found to vary inversely with arterial Po2 between 17 and 55 mmHg. Significant increase in mean adrenal blood flow was not observed at arterial oxygen tensions above about 30 mmHg. 3. Release of physiologically effective amounts of catecholamines from the adrenal medulla occurred only in response to intense hypoxia (arterial Po2 17-1 +/- 2-8 mmHg) and was effectively abolished by section of both splanchnic nerves. Release of pancreatic glucagon in response to such intense hypoxia was unaffected by section of both splanchnic nerves and administration of atropine. In contrast, the rise in plasma pancreatic glucagon concentration during less intense hypoxia was abolished by autonomic blockade. 4. Hypercapnia produced by inhalation of either 5% or 10% CO2 for 30 min stimulated maximal release of adrenal glucocorticoids and caused a substantial rise in plasma glucagon concentration. In contrast, the adrenal medulla was found to be extremely resistant to hypercapnia. Significant release of catecholamines was only observed during intense hypercapnia (inhalation of 10% CO2) and noradrenaline was invariably found to be the predominant amine. 5. The results of these experiments show how endocrine responses to hypoxia and hypercapnia are graded in the conscious calf. Of the mechanisms we have examined the pituitary-adrenal cortical axis is the most sensitive and the adrenal medulla the most resistant, while the pancreatic alpha cell occupies an intermediate position.
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PMID:Adrenal and pancreatic endocrine responses to hypoxia and hypercapnia in the calf. 89 34

Seven men ran at 60% of individual maximal oxygen uptake to exhaustion during beta-adrenergic blockade with propranolol (P), during lipolytic blockade with nicotinic acid (N), or without drugs (C). The total work times (83 +/- 9 (P), 122 +/- 8 (N), 166 +/- 10 (C) min, mean and SE) differed significantly. Epinephrine rose progressively above preexercise levels (0.06 +/- 0.01 ng/ml); at exhaustion concentrations in P experiments (2.15 +/- 0.41) were larger than in N (1.08 +/- 0.31) and C (0.72 +/- 0.28) experiments. Norepinephrine increased consistently while insulin decreased. After an initial decrease glucagon concentrations increased progressively in parallel with declining plasma glucose and were at exhaustion always three times preexercise values. Thus beta-adrenergic blockade did not diminish the glucagon response. Nor was this response increased when alpha-receptor stimulation in P experiments was intensified. Carbohydrate combustion was smaller and NEFA and glycerol concentrations in serum larger during C experiments. Alanine concentrations were never raised at exhaustion. Accordingly, neither stimulation of adrenergic receptors nor NEFA and alanine concentrations are major determinants for the exercise-induced glucagon secretion in man. It is suggested that decreased glucose availability enhances the secretion of glucagon and epinephrine during prolonged exercise.
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PMID:Glucagon and plasma catecholamines during beta-receptor blockade in exercising man. 93 21

Elevation of the intraluminar pressure of rabbit ileum lowers the oxygen supply of the bowel wall in a pressure dependent manner. After decompression local PO2 exceeds the initial values. The infusion of Rheomacrodex-Sorbit induces an increase of local PO2 in the nondistended ileum. The reaction is enhanced in the distended bowel. The application of glucagon does not influence tissue PO2 significantly in either the distended or the undistended bowel. The infusion of Rheomacrodex-Sorbit as well as decompression of the distended bowel are recommended to improve oxygen supply of bowel wall in ileus.
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PMID:[Modification of the oxygen supply of the small intestine demonstrated on the ileus model]. 95 6

Healthy subjects were studied at rest and during 4 h of exercise at approximately 30% of maximal oxygen uptake. At 90 min of exercise 200 g glucose were ingested. A control group was studied during prolonged exercise without glucose administration. Glucose ingestion was followed by a 35% rise in arterial glucose, a 60-70% fall in arterial FFA and glycerol and a two- to threefold rise in arterial insulin. Plasma glucagon, which rose fourfold in controls, failed to rise in the glucose-fed subjects. Glucose uptake by the exercising legs was twofold greater than in controls, accounting for 60% of leg oxygen consumption. Splanchnic glucose output rose rapidly after glucose ingestion to values twice those observed in controls. However, splanchnic uptake of gluconeogenic precursors (lactate, pyruvate and glycerol) fell by 70-100%. Total splanchnic glucose escape after glucose ingestion was 84 +/- 5 g representing 42% of the ingested load. It is concluded that glucose ingestion during prolonged exercise results in a) augmented uptake and oxidation of glucose by the exercising legs, b) diminished lipolysis, c) augmented splanchnic glucose escape in association with decreased hepatic gluconeogenesis, d) retention of half of the ingested glucose within the splanchnic bed, and e) reversal of exercise-induced stimulation of glucagon secretion.
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PMID:Influence of glucose ingestion on fuel-hormone response during prolonged exercise. 99 55

The effect of intravenous injection of 50 mug/kg of glucagon on the hepatic circulation of the pig was studied in 12 animals. Glucagon caused an arterial pressure reduction of 11 mm Hg after two minutes and 7 mm Hg after ten minutes. The portal pressure and blood flow were not altered. The superior mesenteric arterial flow decreased by 12%. The hepatic arterial blood flow increased by 80% after two minutes and by 58% after ten minutes. There was no difference in response when anesthesia was achieved with small intravenous doses of thiopental (Pentothal) sodium or 70% nitrous oxide in oxygen and tubocurarine chloride.
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PMID:Effect of glucagon on hepatic circulation in the pig. 99 4

The cardiac effects of a continuous infusion of glucagon at the rate of 10 mug/min were studied in the Starling heart-lung preparation, modified to measure coronary flow and myocardial oxygen consumption. A maximal increase in myocardial contractility, as reflected by maximal rate of rise of left ventricular pressure, dp/dt, of 31% was observed at a total dose of glucagon of 50 mug and was accompanied by an increase in heart rate and in myocardial oxygen consumption of 59% and 57%, respectively. At a total dose of glucagon of 100 mug, there was an additional and comparable increase only in heart rate and myocardial oxygen consumption of 11.2% and 6.4% respectively. Similarly, at a total dose of glucagon of 150 mug, only heart rate and myocardial oxygen consumption increased additionally by increments of 2.6% and 2.9% respectively. These effects occurred at constant aortic pressure and left ventricular volume. Further infusion of glucagon led to an additional increase only in myocardial oxygen consumption of 4.2%. When the increase in heart rate was largely prevented by prior treatment with veratramine, an increase in dp/dt, not significantly different from the maximal increase obtained with glucagon alone, was accompanied by much lower and closely comparable increases in heart rate and in myocardial oxygen consumption of 15% and 19%, respectively. Coronary flow increased more markedly when glucagon was administered alone and it paralleled the increase in myocardial oxygen consumption. It may be concluded from this study that, in the isolated dog heart preparation, glucagon increases contractility, heart rate and myocardial oxygen consumption and that the increase in myocardial oxygen consumption is related more closely to the increase in heart rate than to the increase in contractility, but a minor increment is referable to a calorigenic action. The increase in coronary flow is of a secondary nature, resulting from the increase in myocardial metabolic demands.
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PMID:The cardiodynamic and metabolic effects of glucagon. 100 38

Elevated intraluminal pressure of rabbit small bowel induces a decrease of tissue pO2 of the bowel wall dependent on the applied pressure. After decompression local pO2 exceeds the initial pO2 values. While the i.v. application of 25 microgram/kg glucagon is not able to improve local oxygen supply of the distended bowel, local pO2 increases considerably after infusion of 7.5 ml/kg dextran 40. Decompression by operation or intestinal tube as well as application of dextran 40 are recommended in the treatment of ileus.
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PMID:[Effects of intraluminal pressure increase on oxygen consumption of the rabbit ileum and its possible pharmacological modification]. 103 28

Radiodiagnostic potential of intra-arterially injected vasodialting agents was investigated by their effect on total and segmenal resistances (VR) of mesenteric vasculature, blood flow in superior mesenteric artery and its bleeding branch; heart rate and ventricular and systemic blood pressure. Dipyridamole, isoxsuprine, protricular and systemic blood pressure. Dipyridamole, isoxsuprine, prochlorperazine, lidocaine, meglumine diatrizoate and carbon dioxide were poor dilators. Phentolamine produced hypotension; glucagon and serpasil an extremely long dilation. A large and short vasodilation was produced with tolazoline and nylidrin, but both agents increased VR of the postcapillary segment and caused transient hypotension and arrhythmias, nylidrin's side effects were smaller. Oxygen produced large and long vasodilation and minimal systemic effects. It is concluded that oxygen or possibly nylidrin are suitable agents should an intermittently bleeding mesenteric artery be dilated for diagnostic purposes prior to angiography.
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PMID:Vasocilators in the canine mesenteric circulation. Evaluation of a potential aid in the diagnosis of gastrointestinal bleeding. 108 28


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