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

1. The mechanism of action of glucagon and epinephrine was studied in perfused rat livers. Hormone-induced transitions from one metabolic steady state to another were followed in a non-recirculating perfusion system. Glucose and lactate production rates, oxygen uptake and K+ redistribution were measured. 2. Glucagon (3 nM), cyclic AMP (0.2 mM) and epinephrine (0.5 muM) had similar effects on K+ concentrations in the perfusate. Glycogenolysis responded more rapidly and O2 uptake was enhanced to a larger extent with epinephrine than with the other agents. alpha- and beta-receptor responses were differentiated by the use of phenylephrine (0.5 muM), isoproterenol (0.5 muM) and adrenergic blocking agents (phentolamine and beta-blocker Ro 3-4787 at 0.1 mM). 3. alpha-receptors mediated an activation of glucose production that was very rapid and was paralleled by a transient decrease of K+ concentrations in the effluent from the liver, lactate production rose gradually. Respiration was also enhanced, but fell again as lactate production increased. 4. beta-receptor stimulation was followed by an increase of glucose production that was less drastic and was paralleled by a K+ release, lactate production and respiration were only slightly enhanced. beta stimulation and glucagon both resulted in an inhibition of the alpha-adrenergic effect on lactate release and simultaneously increased O2 uptake. 5. We concluded that in perfused rat livers alpha- as well as beta-adrenergic receptor stimulation resulted in an activation of glycogenolysis, possibly by two different mechanisms.
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PMID:Metabolic responses of perfused rat livers to alpha- and beta-adrenergic agonists, glucagon and cyclic AMP. 24 Apr 32

Acute glucagon treatment of intact rats has been found to cause a stimulation of hepatic mitochondrial respiration as measured by monitoring oxygen uptake polarographically. Rates of State 3 respiration with several NAD-linked substrates and succinate were increased significantly after hormonal treatment and isolation of mitochondria. This stimulation cannot be ascribed to a partial uncoupling effect since State 4 respiration as measured by monitoring oxygen uptake polarographically. Rates of State 3 respiration with either slightly increased or unchanged. Furthermore, rates of uncoupled respiration with these substrates were also stimulated after hormonal treatment. On the other hand, respiratory rates (State 3, 4, and uncoupled) with ascorbate-N,N,N',N'-tetramethyl-p-phenylenediamine as substrate were unaffected by glucagon treatment. The hormonally stimulated rates of respiration produced a corresponding increase in the rate of generation of high energy state as indicated in measurements of Ca2+ uptake by isolated mitochondria. Rates of Ca2+ uptake were monitored by two methods: measurement of initial rates of proton ejection following CaCl2 additions and measurement of disappearance of Ca2+ from the suspension medium using murexide as indicator in a dual wavelength spectrophotometer. A significant stimulation in the initial rate of succinate-dependent Ca2+ uptake was noted after glucagon treatment of animals and isolation of hepatic mitochondria. No effect of the hormonal treatment was seen on the extent of Ca2+ uptake or the stoichiometry of H+ ejected per Ca2+ taken up. That the hormonal effect on Ca2+ transport is at the level of the substrate-induced generation of high energy state is indicated by the observation that no effect of glucagon treatment is seen on ATP-dependent Ca2+ uptake. Glucagon-induced changes in the activities of substrate-metabolizing enzymes are considered unlikely for the following reasons: (a) previously published data showed a lack of a hormonal effect on pyruvate-metabolizing enzymes and (b) data in this study showing no effect of glucagon treatment on the activity of NAD-malate dehydrogenase as measured in mitochondrial lysates. All of these observations are consistent with either an activation of mitochondrial substrate transport and/or a stimulation of mitochondrial electron transport by glucagon treatment. Regardless of the exact mechanism involved, the effect of the hormonal treatment is to produce an increase in ATP synthetic and ion-pumping capability during a period of increased energy demand, i.e. increased gluconeogenesis.
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PMID:Glucagon stimulation of mitochondrial respiration. 24 Aug 44

The calorigenic action of glucagon was studied in several species by measuring its effect on the oxygen comsumption. The calorigenic effect was most pronounced in the quail and also evident in young adult rats of two different strains but not in mice and guinea pigs. The influence of various drugs on the calorigenic effect of glucagon was investigated in rats. Ganglionic blocking agents (hexamethonium, mecamylamine, chlorisondamine) as well as adrenergic blocking drugs (propranolol, butoxamine, phentolamine) greatly reduced the glucagon-induced calorigenesis but after pretreatment with reserpine, guanethidine or chemical sympathectomy with 6-hydroxydopamine the calorigenic effect of glucagon was exaggerated. It was somewhat diminished by nicotinic acid but not by chlorpromazine or lithium and potentiated by cocaine but not by theophylline.--These results are not indicative for an involvement of adenly cyclase--cyclic AMP--system in glucagon-induced calorigenesis but they are compatible with the assumption that the hormone enhances the metabolic rate by releasing catecholamines from the adrenal medulla.
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PMID:[The calorigenic effect of glucagon]. 24 4

Preoperative and serial postoperative clinical, cardiovascular, physiologic, and metabolic studies were carried out on 86 patients undergoing coronary artery bypass surgery (CABG); and 48 patients undergoing abdominal general surgical procedures (GSEL). Multivariable statistical analysis of these data showed the patients to be in different physiologic states and to manifest several types of recovery trajectories that could not be discerned on clinical grounds alone. The CABG patients followed one of three types of cardiogenic recovery trajectories. In contrast, GSEL patients show a normal recovery trajectory different from all CABG types. When sepsis develops, and exaggerated stress response (A state) occurs, with increased oxygen consumption and a pattern of amino acids, fat, and glucose breakdown products, which is heightened but similar to the response of nonseptic GSEL patients. With progression of sepsis severity, an unbalanced hyperdynamic recovery trajectory (B state) develops in which a decrease in oxygen consumption is associated with increases in the aromatic amino acids tyrosine, tryptophane, and phenylalanine; and decreases in the branched-chain amino acids, leucine and isoleucine. Triglycerides rise as keto acids fall, but both lactate and pyruvate rise. Glucagon is persistently high, regardless of insulin levels. The quantifiably different physiologic recovery trajectories reflect altered hormone and metabolic states and imply different responses to therapy.
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PMID:The physiologic recovery trajectory as the organizing principle for the quantification of hormonometabolic adaptation to surgical stress and severe sepsis. 31 78

To examine gut-islet interrelationships, we entirely separated the gastrointestinal tract from the rat. When we arterially perfused this preparation with an erythrocyte-free solution for 1 h, it remained histologically intact and took up oxygen and glucose. Feedings were given via a duodenal tube. The gut absorbed glucose when glucose in the feeding was high (9.2 g/dl), but not when glucose in the feeding was low (58 mg/dl). With feeding, the portal venous effluent (PVE) from this preparation (stomach to ileum) enhanced late-phase, glucose-induced insulin secretion from pancreas of another rat. This enhancement occurred when the gut was fed either glucose (9.2 g/dl) in electrolyte solution or electrolyte solution alone. PVE from glucose-fed upper gut (stomach, duodenum) was similarly insulinotropic. In contrast, PVE from unfed gut or from glucose-fed gut of old rats was not insulinotropic. PVE from all gut preparations except upper gut produced a glucagon "spike" during basal pancreatic perfusion. Effects of gastrointestinal peptides (gastric inhibitory polypeptide, cholecystokinin octapeptide, secretin, gastrin) and immunoassays of PVE suggested that the insulinotropic substance is not one of these peptides. Thus, an insulinotropic substance that is not dependent on feeding nutrient material is secreted from the intestine.
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PMID:Secretion of an insulinotropic factor from isolated, perfused rat intestine. 37 52

New concepts concerning the pathogenesis and therapy of diabetic ketoacidosis are reviewed. The regulation of ketogenesis by intrahepatic enzymic processes and the roles of insulin deficiency or glucagon or other counterregulatory hormone excess are summarized. Major emphasis is placed on an analysis of the use of low-dose insulin regimens for the treatment of ketoacidosis. Most patients with diabetic ketoacidosis will respond to low-dose, hourly, intravenous or intramuscular regular insulin. Low doses of insulin are as effective as high doses and have fewer associated complications of hypoglycemia and hypokalemia. Phosphorus deficiency is common in diabetic ketoacidosis and hypophosphatemia usually becomes manifest within 4 to 12 h of institution of therapy. Phosphorus supplementation is now generally recommended to replete erythrocyte 2,3-diphosphoglycerate and improve oxygen delivery to tissues. Coexistent and biochemically significant lactic acidosis is a relatively infrequent complication of diabetic ketoacidosis and when present is usually due to underlying disorders associated with poor tissue perfusion.
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PMID:Diabetic ketoacidosis: new concepts and trends in pathogenesis and treatment. 41 52

Plasma glucagon and catecholamines increase during prolonged submaximal exercise, but the magnitude of the increase is less in endurance-trained individuals than in untrained subjects. We have studied the rapidity at which this adaptation occurs. Six initially untrained healthy subjects exercised vigorously (on bicycle ergometers and by running) 30-50 min/day, 6 days/wk, for 9 wk. Prior to the beginning of training and at 3-wk intervals thereafter, participants were subjected to 90-min bicycle ergometer test work loads that elicited 58 +/- 2% of the subjects' initial maximal oxygen consumption. The major proportion of the training-induced decrement in plasma glucagon and catecholamine responses to exercise was seen after 3 wk of training. We conclude that the hormonal component of the training adaptation occurs very early in the course of a vigorous endurance training program.
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PMID:Training-induced changes in hormonal and metabolic responses to submaximal exercise. 45 55

Levamisole at a concentration of 10(-3)M inhibits the oxygen consumption of resting platelets, the thrombin induced burst and the platelet aggregation induced by ADP. At the concentration of 10(-7)M it exerts still an inhibitory activity of the thrombin induced burst, but it does not inhibit neither the basal oxygen consumption nor the platelet aggregation. At every tested concentration platelet survival in the presence of levamisole is comparable to that of controls. Levamisole moreover, together with theophylline and glucagon, shows a synergistic inhibiting influence toward the burst of oxygen consumption. Our data suggest that levamisole may act by producing an enzymatic block of cyclo-oxygenase.
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PMID:In vitro effect of levamisole on oxygen consumption and survival of platelets. 49 15

In an isolated rat liver perfusion system the effects of normothermal ischemia on hepatic functions were investigated. After 30 minutes of anoxy bile production and BSP elimination capacity of the liver are significantly reduced. The quantity of secreted "ascites" from the surface of the liver several times high after anoxic damage, while oxygen consumption, portal venous pressure and ammonia elimination do not differ significantly from the controls. Pretreatment with insulin plus glucose, isoproterenol, hypoxanthine, chlorpromazine and glucagon (5 micrograms/100 g i.v., or 0.2 mg/100 g s.c.) does not reduce noticeably the normothermal anoxic lesion of the liver Glucagon (50 micrograms/100 g i.v.), allopurinol, dibenzyline, ATP-MgCl2 and aspartic acid enhance significantly the ischemia-tolerance of liver in vitro.
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PMID:Ischemic damage of the liver. Part I: In vitro investigation of the prevention of the ischemic lesion of the liver. 49 24

We compared the effectiveness of three pharmacologically and chemically dissimilar vasodilators (histamine, glucagon, and perhexiline) in reversing the hemodynamic and metabolic deficits of intestinal ischemia produced by hemorrhage. With intraarterial infusion into the superior mesenteric artery of anesthetized control dogs, all three agents increased mesenteric blood flow and oxygen consumption without altering systemic arterial blood pressure. Similarly, in the ischemic gut following moderate hemorrhage all three vasodilators increased mesenteric flow and oxygen consumption while reducing vascular resistance and not affecting systemic arterial blood pressure. On a molar basis glucagon was the most potent dilator drug. In severely hemorrhaged dogs whose intestinal blood flow had been reduced nearly 80%, glucagon restored oxygen uptake and vascular resistance to control levels. These findings demonstrate the efficacy of three different vasodilators in reversing the mesenteric ischemia and hypoxia produced by hemorrhage.
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PMID:Effects of vasodilators on mesenteric ischemia and hypoxia induced by hemorrhage. 49 29


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