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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 intravenous somatostatin on blood levels of metabolites and hormones has been examined in normal subjects who performed a 30-minute period of bicycle exercises at 70% maximal exercise capacity. The results have been compared with control studies in the same subjects. Measurements were made of blood levels of lactate, glucose, free fatty acids, glycerol, acetoacetate, 3-hydroxybutyrate, insulin, glucagon, growth hormone (hGH) and prolactin. Growth hormone and glucagon release were suppressed during exercise with somatostatin and there was a subsequent elevation during recovery. There was slight post-exercise depression of insulin, but no alteration of plasma prolactin secretion. Blood glucose was reduced during exercise with somatostatin and increased during recovery. The elevation of ketone bodies after exercise was greater in the investigation with somatostatin, but there were no significant changes in other metabolites. Somatostatin, although causing inhibition of hGH release, appeared to have no significant effect upon fatty acid mobilization during exercise.
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PMID:The effect of somatostatin on metabolic and hormonal changes during and after exercise. 47 77

The significance of glucagon for post-exercise glucose homeostasis has been studied in rats fasted overnight. Immediately after exhaustive swimming either rabbit-antiglucagon serum or normal rabbit serum was injected by cardiac puncture. Cardiac blood and samples of liver and muscle tissue were collected before exercise and repeatedly during a 120 min recovery period after exercise. During the post-exercise period plasma glucagon concentrations decreased but remained above pre-exercise values in rats treated with normal serum, while rats treated with antiglucagon serum has excess antibody in plasma throughout. Nevertheless, all other parameters measured showed similar changes in the two groups. Thus after exercise the grossly diminished hepatic glycogen concentrations remained constant, while the decreased blood glucose concentrations were partially restored. Simultaneously concentrations in blood and serum of the main gluconeogenic substrates, lactate, pyruvate, alanine and glycerol declined markedly. During the post-exercise period NEFA concentrations in serum and plasma insulin concentrations remained increased and decreased, respectively, while plasma catecholamines did not differ from basal values. Muscle glycogen concentration decreased slightly. These findings suggest that in the recovery period after exhausiive exercise the increased glucagon glucagon concentrations in plasma do not influence gluconeogenesis.
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PMID:Lak of influence of glucagon on glucose homeostasis after prolonged exercise in rats. 56 4

Metabolic adaptations to cyclic patterns of food intake were studied in genetically lean and obese Zucker rats. Twenty-four lean and 24 obese rats were exposed to 12 hours of light and 12 hours of dark and allowed food ad libitum. Both groups of rats ate more during the dark period of the cycle. The obese consumed nearly twice as much food as the lean during the light period of the cycle. At 4-hour intervals, rats were killed and liver and epididymal fat pads were removed for metabolic studies. Adipose tissue from lean rats demonstrated marked changes in rates of lipogenesis during the 24-hour cycle whereas adipose tissue from obese rats maintained a relatively steady rate of lipogenesis. Glucose incorporation into the glycerol moiety of triacylglycerol was nearly 3-fold higher in adipose tissue from obese rats. Liver lipogenesis in lean and obese rats followed their food intake pattern. Liver lipogenic rate (expressed per organ) was 3- to 5-fold higher in obese than lean rats during most of the 24-hour cycle. These data support the concept that the excessive fatty acids produced in the liver of obese rats are being esterified by adipose cells. Lipolytic response to glucagon was found in adipose tissue from obese rats during the dark and light periods, but only during the dark period for lean rats. These data suggest, in comparison to lean rats, that obese rats do not enter a relative catabolic state during a 24-hour cycle. A constant anabolic state in the genetically prone individual may lead to excessive lipid deposition and obesity.
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PMID:Diurnal changes in adipose and liver tissue metabolism of lean and obese Zucker rats. 57 Oct 11

The effect of 10 mM fluoride on glycerol production in vitro from rat epididymal adipocytes was investigated. Fluoride had no effect on the basal glycerol production, irrespective of the presence or absence of Ca++ and Mg++ ions. When stimulating the glycerol production with 10 mM theophylline, fluoride reduced the stimulation in the absence of either Ca++ or Mg++ or both. In the presence of both ions, fluoride had no effect on the theophylline stimulation. Fluoride also reduced the stimulative effect of adrenaline on glycerol production, but not that of glucagon. Increased adrenaline concentration could not overcome the inhibitory effect of fluoride.
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PMID:Effect of fluoride on glycerol production in rat adipocytes in vitro. 57 58

The importance of autonomic nervous activity for the pancreatic hormonal response to exercise in man was studied. 7 men ran at 58% of V(O2)max (determined without administration of drugs) to exhaustion during alpha-adrenergic blockade with phentolamine (P), during parasympathetic blockade with atropine (A), or without drugs (C). At rest phentolamine increased the plasma concentrations of both insulin and norepinephrine. During exercise norepinephrine concentrations increased and were in P experiments 3 times the concentrations in C experiments. Insulin always declined during exercise but in P experiments never decreased below basal levels. At identical times neither glucagon nor glucose differed significantly in the different expts. Thus during exercise alpha-adrenergic blockade increased insulin concentrations but did not diminish the glucagon response. Nor was this response increased when beta-receptor stimulation in P experiments was intensified by the particularly high catecholamine concentrations. The concentrations of FFA, glycerol and lactate were highest in P experiments and identical in A and C experiments. These findings indicate that during prolonged moderate exercise in man insulin secretion is depressed by stimulation of alpha-adrenergic receptors whereas glucagon secretion is not influenced by adrenergic receptors. Stimulation of beta-adrenergic receptors enhances lipolysis but neither lipolysis nor pancreatic hormonal secretion is influenced by cholinergic activity during exercise.
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PMID:Catecholamines and pancreatic hormones during autonomic blockade in exercising man. 59 18

1. In incubated tubule fragments from renal cortex of fed rats gluconeogenesis from pyruvate was stimulated by adrenaline (1mum optimum) and by the selective alpha-adrenergic agonists oxymetazoline and amidephrine. The selective beta-agonists isoproterenol and salbutamol were ineffective at concentrations up to 10mum. 2. Stimulation of gluconeogenesis by 1mum-adrenaline was almost completely blocked by 10mum-phentolamine (alpha-antagonist), partially blocked by 10mum-phenoxybenzamine (alpha-antagonist) and unaffected by 10mum-propranolol (beta-antagonist). 3. Adrenaline stimulation of gluconeogenesis was rapid and was sustained for at least 1h. 4. Oxymetazoline (alpha-agonist) was extremely potent in stimulation of gluconeogenesis. This compound stimulated glucose production from pyruvate, lactate and glutamate, but not from succinate or glycerol. 5. In the absence of Ca(2+) oxymetazoline was ineffective, whereas some stimulatory effect of adrenaline on gluconeogenesis was still observed. 6. Glucagon had no effect on gluconeogenesis from pyruvate in the presence of 1.27mm-Ca(2+) and inhibited the process in the presence of 0.25mm-Ca(2+). Parathyrin (parathyroid hormone) stimulated gluconeogenesis at 1.27mm-Ca(2+). 7. In short incubations of tubule fragments glucagon, papaverine and adrenaline significantly increased 3':5'-cyclic AMP. Adrenaline also slightly decreased 3':5'-cyclic GMP. Oxymetazoline had no effect on the amount of either cyclic nucleotide. 8. At all concentrations tested, theophylline and papaverine decreased gluconeogenesis from pyruvate. 9. It is concluded that renal gluconeogenesis may be increased by alpha- but not beta-adrenergic stimuli and that this is probably independent of changes in 3':5'-cyclic AMP or 3':5'-cyclic GMP. An involvement of Ca(2+) in the action of oxymetazoline appears likely, but this is less certain with adrenaline.
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PMID:Hormonal control of gluconeogenesis in tubule fragments from renal cortex of fed rats. Effects of alpha-adrenergic stimuli, glucagon, theophylline and papaverine. 59 61

Spontaneous fasting hypoglycemia developed in four nondiabetic patients with end-stage renal failure. All were undergoing long-term maintenance hemodialysis and three patients were anephric. Hypoglycemia was generally accompanied by severe metabolic acidosis and, in three patients, lactic acidemia. Abnormalities of hepatic structure and/or function were present in three patients. In one patient, hypoglycemia was refractory to exogenous glucagon, failed to respond to alanine, glycerol, or galactose, and was associated with suppressed plasma insulin and elevated plasma glucagon levels. Fasting hypoglycemia appeared to result from several mechanisms. In at least two patients, fasting hypoglycemia and lactic acidosis resulted from impaired hepatic gluconeogenesis in association with impaired or absent renal glucose production. Additionally, substrate limitation probably contributed to hypoglycemia in several patients.
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PMID:Spontaneous hypoglycemia in chronic renal failure. 68 26

Previous findings that 2.5 mM quinolinic acid inhibits gluconeogenesis more strongly from alanine than from lactate have been confirmed. 15 mM quinolinic acid completely inhibited gluconeogenesis from lactate as well as from alanine whereas the formation of glucose from fructose and the production of urea from ammonia and lactose were not affected. The pattern of the gluconeogenic intermediates was the same in the presence of 15 mM quinolinic acid as with 2.5 mM of the inhibitor. It is concluded that high as well as low concentrations of quinolinic acid inhibit gluconeogenesis at the step between oxaloacetate and phosphoenolpyruvate. Furthermore, 5-methoxyindole-2-carboxylic acid, an inhibitor of mitochondrial pyruvate metabolism, also completely blocked gluconeogenesis from lactate whereas glycerol conversion to glucose was only weakly inhibited. All these results do not support the concept of an alternate pathway of gluconeogenesis from lactate proposed by others. 2.5 mM quinolinic acid also partially blocked the formation of urea from alanine. It is suggested that quinolinic acid may have a second site of action causing an inhibition of the glutamate-pyruvate transamination owing to lack of 2-oxoglutarate in the cytosol. In the presence of quinolinic acid, glucagon caused about the same increase in aspartate and malate tissue levels in the absence of added substrates as in the presence of added lactate or alanine. Therefore, no additional effect of glucagon on gluconeogenesis from lactate or alanine prior to the block by quinolinic acid could be demonstrated.
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PMID:Effects of quinolinic acid and glucagon on gluconeogenesis in the perfused rat liver. 69 6

Most forms of liver disease are probably associated with impaired gluconeogenesis, although hypoglycaemia is rarely an important clinical feature. Blood concentrations of the gluconeogenic precursors, lactate, glycerol and alanine are elevated although, in certain situations, alanine levels may be decreased. Abnormal glucose tolerance is present in both acute and chronic liver disease, but is usually not of clinical importance. The mechanism of glucose intolerance remains uncertain, with diminished hepatocyte mass, portal diversion and insulin resistance the major postulates. Indeed, the importance of the liver in disposing of an oral glucose load, is still questioned. Both hyperinsulinism and hypoinsulinism are found in liver disease, with hyperinsulinism common in cirrhosis and acute viral hepatitis. This is accompanied by insulin resistance. The hyperinsulinism is probably due to defective hepatic clearance of insulin rather that to over-production. The cause of the insulin resistance remains to be established. Glucagon levels are raised and may contribute to this resistance. Growth hormone levels are also increased but are associated with low somatomedin levels and the role of growth hormone in insulin resistance is therefore questionable. Future developments include use of new animal models, studies of biopsy specimens and studies of hepatic hormone receptors.
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PMID:Carbohydrate metabolism in liver disease. 79 84

To evaluate the role of glucagon in the pathogenesis of diabetic ketoacidosis in man, we studied the effect of suppression of glucagon secretion by somatostatin on changes in plasma beta-hydroxybutyrate and glucose concentrations (as well as changes in their precursors) after acute withdrawal of insulin from seven patients with juvenile-type diabetes. Suppression of glucagon secretion prevented the development of ketoacidosis for 18 hours after acute insulin withdrawal, whereas in control studies mild ketoacidosis occurred 10 hours after insulin was stopped. Plasma beta-hydroxybutyrate, glucose, free fatty acid, and glycerol levels were all markedly lower during suppression of glucagon secretion (p smaller than 0.001), whereas plasma alanine levels were higher (p smaller than 0.001). These studies indicate that insulin lack per se does not lead to fulminant diabetic ketoacidosis in man and that glucagon, by means of its gluconeogenic, ketogenic, and lipolytic actions, is a prerequisite to the development of this condition.
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PMID:Prevention of human diabetic ketoacidosis by somatostatin. Evidence for an essential role of glucagon. 80 37


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