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)

In diabetics with different therapy indications the effect of the treatment on the lipid parameters of blood was examined. We estimated the change of the triglycerides, the cholesterol, the free fatty acids and the glycerol depending on the duration of the therapy. We used a combined stimulation test (combination of 100 g glucose, 1.0 g tolbutamide and 1.0 g glucagon in temporary coupling) as method for characterization of the type of diabetes. At the beginning of the therapy the fat parameters mentioned did not differ in patients with exclusively dietetic treatment and in SuH-patients. After longer duration of the therapy in exclusively dietetically compensated patients the fasting glycerol values decreased, were, however, statistically not significant. There were also no essential changes of the triglycerides, the cholesterol and the values of the free fatty acids in the two forms of treatment. The improvement of the carbohydrate tolerance could not be explained with changes of the insulin secretion. The results plead for the fact that the improvement of the diabetic metabolism develops by an increase of the peripheral insulin effectivity. The behaviour of the lipid parameters is not sufficient for an explanation of the carbohydrate tolerance.
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PMID:[Effect of diabetes therapy on the lipid parameters in blood]. 91 May 22

Chloralose-anaesthesized dogs, starved for 24 hours, were used to determine the effects of 10 microgram/kg glucagon, administered i.v. as a single bolus injection, on liver substrates in situ (glycogen, glucose-1-phosphate, glucose-6-phosphate, glucose, fructose-6-phosphate, fructose-1,6-diphosphate, triose phosphates, glycerol-3-phosphate, phosphoenolypyruvate, pyruvate, lactate, citrate, malate, ATP, ADP, and AMP). liver samples were obtained by instant deep-freezing with Wollenberger clamps on four consecutive occasions at 10-minute intervals. Heart rate and blood pressure were continuously monitored. Serial liver sampling per se had no significant effects on liver metabolism or systemic haemodynamics in a group of control animals. In a second group glucagon, administered after the initial freeze-clamp sampling to obtain baseline values, led to a marked activation of the glycogenolytic pathway resulting in glucose release from the liver.
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PMID:Effects of glucagon on liver metabolism in intact dogs. 92 72

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

1. Six well-trained cyclists and six untrained subjects were studied during and immediately after four successive 7 min periods of exercise at 30, 45, 60 and 75% of their maximal work capacity. 2. Venous blood samples were taken at rest, at the end of each exercise period and 5 min following the end of exercise, for estimation of metabolites in blood and plasma insulin, growth hormone, cortisol and catecholamines. 3. The results showed significant differences in the mobilization and utilization of muscle fuels between the athletically fit cyclists and the untrained group. In the cyclists, glucose, glycerol and free fatty acid concentrations were higher, but lactate, pyruvate and alanine were lower than in the untrained subjects during exercise. 4. Plasma catecholamines rose in both groups during exercise but the rise was significantly less in the racing cyclists. Plasma insulin was depressed to a greater extent in the untrained subjects during exercise and plasma glucagon rose to a greater extent during strenuous exercise and remained elevated after the end of exercise in the untrained group. Plasma human growth hormone rose to a greater extent during exercise and remained elevated after the end of exercise in the untrained group. Plasma cortisol fell at low and moderate exercise rates in both groups, but to a smaller extent in the cyclists. Cortisol values rose at higher workloads and were significantly higher in the cyclists at the end of exercise. 5. It is concluded that there are significant differences in the metabolic and hormonal responses to exercise between athletically trained and untrained individuals, even when the physically fit subjects work at the same percentage of their maximal capacity as the unfit subjects.
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PMID:Differences in the metabolic and hormonal response to exercise between racing cyclists and untrained individuals. 94 45

The significance of glucagon for the alterations in carbohydrate and fat metabolism during swimming has been evaluated. Fed, male rats were used. Blood was drawn by cardiac puncture for glucose analysis and either rabbit-antiglucagonserum (A-rats) or normal rabbitserum (N-rats) injected. Twenty-nine rats were then forced to swim (S-rats) with a tail weight for 60 min, while 16 rats were resting controls (C-rats). Subsequently blood was drawn and samples of liver and muscle tissue collected. In SN-rats glucagon concentrations increased from 152 +/- 18 (S.E.) pg/ml (CN-rats) to 332 +/- 61 (P less than 0.05), while liver glycogen decreased (P less than 0.001) and blood glucose increased (P less than 0.05). In SA-rats, however, the changes in liver glycogen and blood glucose were halved indicating that increased glucagon secretion enhances hepatic glycogen depletion during prolonged exercise. NEFA rose in SA-rats (P less than 0.005) as well as in SN-rats (P less than 0.05). Glycerol concentrations, however, only increased in SA-rats (P less than 0.05) indicating a shift towards lipid combustion in antibody treated rats. Muscle glycogen and plasma insulin diminished and blood lactate increased uniformly in exercised rats.
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PMID:The influence of glucagon on hepatic glycogen mobilization in exercising rats. 94 10

Human liver tissue was obtained as surgical biopsies in 29 subjects operated on for uncomplicated gallstone disease. Liver slices were incubated in Krebs-Ringer bicarbonate buffer solution, pH 7.4, with 17 l-amino acids, lactate, glycerol, and glucose at various concentrations. The incorporation rate of alanine, lactate, and glycerol into glucose, glycogen, and CO2 was determined by use of 14C-labeled precursors. The gluconeogenetic rate of all substrates was increased 10-35 times by increasing precursor concentration in the medium. Insulin at a physiological concentration (300 mU/l) and dexamethasone (0.001 mmol/l) had slight but significant effects on the incorporation rate of alanine into glucose and glycogen, respectively. Glucagon had no effect. Glucose in the incubation medium did not influence the incorporation rate of precursors into glucose, glycogen, or CO2, suggesting that glucose was not of importance for the regulation of the gluconeogenesis. The gluconeogenetic rate of a precursor was not dependent on or influenced by the presence of other precursors. The gluconeogenesis in human liver slices at physiological concentrations of precursors was 5-20% of the maximal rate reported for the rat liver. When the precursor concentration in the medium was increased, the gluconeogenetic rate increased to values close to those reported for the rat liver in vitro and for man in vivo. This in vitro preparation of human liver seems to be valid for evaluation of gluconeogenesis in man.
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PMID:Gluconeogenesis in human liver tissue. An in vitro method for evaluation of glyconeogenesis in man. 95 52

The importance of glucagon in the regulation of carbohydrate metabolism is clearly established. However, the role played by this hormone in the regulation of the overall fuel economy is less certain, particularly with respect to such nonglucose fuels as free fatty acids, glycerol, and ketoacids. In order to elucidate glucagon's role with respect to the latter substrates, dogs were infused with solutions of these three fuels, and their A-cell responses to concomitant insulin-induced hypoglycemia were studied. In addition, epinephrine levels were also monitored. It was found that while these infusions failed to suppress glucagon release, the ketoacid infusion did significantly reduce epinephrine secretion during the insulin-induced hypoglycemic period. It was therefore concluded that glucagon secretion under these experimental conditions is not responsive to prevailing non-glucose fuel levels. Indeed, these data suggest that the sympathetic nervous system may play an important role in the regulation of the over-all fuel economy.
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PMID:Effects of beta-hydroxybutyrate, glycerol, and free fatty acid infusions on glucagon and epinephrine secretion in dogs during acute hypoglycemia. 96 13

Adipose tissue was removed from five-day old chickens after a) an overnight fast, b) total pancreatectomy and c) partial evisceration and digested with collagenase. The adipocytes were incubated with pancreatic glucagon (Novo) and the glycerol released into the medium taken as the index of lipolytic activity. A moderate fast, while being without effect on basal lipolysis, slightly decreased adipocyte sensitivity to glucagon. Pancreatectomy and evisceration significantly reduced both basal lipolysis and the response to glucagon: the impairment was most evident just at the concentration found in the plasma of such operated animals. It seems clear that normal lipolysis is under the control not only of pancreatic factors, but also of those of intestinal origin, and can only proceed normally when both are present.
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PMID:The contribution of the pancreas and the intestine to the regulation of lipolysis in birds. 2. Impaired lipolytic activity of pancreatic glucagon in the absence of either the pancreas or the intestine in the chicken. 97 34

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

By measuring the specific radioactivity of glucose released from isolated perfused livers of normal, fed rats in the presence of [U-14C]fructose, the gluconeogenetic and glycogenolytic contributions to glucose production were estimated. After 20 min of perfusion with 4 mM fructose, glycogenolysis was inhibited by 40% in the absence and by 70% in the presence of glucagon (3 nM). Glucagon decreased the release of lactate plus pyruvate and enhanced glucose formation from fructose without affecting its uptake. Glycerol (4 mM) and xylitol (3 mM) had qualitatively similar, but smaller effects on glucagon-stimulated glycogenolysis. The glucagon-mediated phosphorylase b to a conversion was not altered by fructose, indicating that glycogenolysis was decreased as a consequence of an inhibition of phosphorylase a. During the first minutes after the addition of fructose, decreased ATP/AMP ratios and tissue Pi levels correlated with a transient increase of phosphorylase a activity. It was concluded that the effects of fructose on the control of hepatic glycogenolysis and glucose production were the result of a complex interplay between a transient b to a conversion of phosphorylase and an inhibition of the a-form of the enzyme, possibly by fructose 1-phosphate and other phosphorylated metabolites.
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PMID:Interactions of glucagon and fructose in the control of glycogenolysis in perfused rat liver. 100 7


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