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

The Zucker (fatty) rat is one of a group of animals that inherit obesity as an autosomal Mendelian recessive trait. These rats are obese, hyperphagic, and hyperinsulinemic, but blood glucose remains at normal levels. Although these rats eat more than normal rats, their response to the addition of adulterants to the food or after exposure to the cold is more like that of normal rats than rats with hypothalamic obesity. The hypertriglyceridemia which characterized these animals is due to the increased hepatic production of a very low density lipoproteins. Adipocytes are increased in size and in number with the subcutaneous fat depot showing the largest increase in the number of fat cells. Lipogenesis from glucose is brisk in the young animals but declines with age. Enzymatic patterns of glycolysis and gluconeogenesis appear to reflect the altered internal milieu rather than specific defects. Endocrine changes in the fatty rat include hyperinsulinemia, reduced levels of glucagon, hypothyroidis, and impaired reproductive function. A model is presented in which the features of the genetically obese (Zucker) fatty rat are compared with those of animals with hypothalamic obesity.
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PMID:The Zucker-fatty rat: a review. 32 51

Variations in concentrations of growth hormone, insulin, glucagon, prolactin, adrenal corticoids, and thyroid hormones in blood plasma of ruminants as related to circadian rhythms, environmental factors and nutrition are reviewed. Rhythms in prolactin concentrations are related to light and temperature. Concentrations of prolactin in plasma are higher in warm environments and during longer photoperiods. There is episodic secretion of growth hormone in cattle with frequent peaks in plasma concentrations during 24 h. Marked increases in environmental temperature result in greater secretion of growth hormone for short times followed by a decline in plasma concentration with prolonged exposure. Extreme cold temperature also increases growth hormone concentrations in plasma. Secretion of thyroid hormones increases in cold and decreases in warm environments. Circadian rhythms are definite for plasma concentrations of adrenal corticoids in ruminants adjusted to their surroundings. Peaks occur late in dark periods, and lows occur during the end of light periods. Circadian patterns have not been consistent for secretion of insulin. Prolonged subjection to stresses such as noise, handling, and restraint can modify concentrations of prolactin, growth hormone, and adrenal corticoids. Changes in concentrations of insulin may occur if blood glucose is increased. After feeding, concentrations of growth hormone in plasma decrease and concentrations of insulin and glucagon increase. Relationships of these changes with metabolism are discussed.
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PMID:Relation of hormonal variations to nutritional studies and metabolism of ruminants. 35 Sep 15

The relationship between thermoreception, hormonal secretion and muscular activity was studied. 6 men swam 60 min in 21, 27 and 33 degrees C water at a speed requiring 68% of VO2 max (determined in 27 degrees C water). Rectal temperature increased in 33 degrees C (1.3 +/- 0.2 degrees C, mean and S.E.) and 27 degrees C (0.7+/- 0.1 degrees C) expts. but decreased in 21 degrees C expts. (0.8 +/- 0.3 degrees C). Changes in esophageal and muscle temperatures parallelled changes in rectal temperature. Plasma noradrenaline was higher in 33 degrees C than in 27 degrees C expts. and growth hormone, cortisol and glucagon concentrations increased in 27 degrees C and 33 degrees C expts. only. Insulin concentrations were uniformly depressed during swimming at the different water temperatures. In 21 degrees C expts. noradrenaline and adrenaline concentrations were higher than in 27 degrees C expts. VO2, carbohydrate combustion and peak lactate were slightly lower in 33 degrees C expts. Plasma glucose decreased slightly and FFA and glycerol concentrations increased identically in all expts. Heart rate increased continuously during swimming in 27 degrees C and 33 degrees C expts., but not in 21 degrees C expts. In conclusion the rise in body temperatures normally observed during exercise enhances the exercise induced increases in the plasma concentrations of noradrenaline, cortisol, growth hormone and glucagon. Decreased body temperatures may elicit catecholamine secretion as a direct consequence of thermoreception. Shivering may account for previously observed decreases in insulin secretion during cold stress but not for increases in cortisol and growth hormone.
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PMID:The effect of water temperature on the hormonal response to prolonged swimming. 44 63

Heat production of isolated brown-fat cells by addition of noradrenaline and glucagon was measured in warm-acclimated control, cold-acclimated and heat-acclimated rats by use of a twin-type conduction microcalorimeter. Noradrenaline and glucagon induced maximum heat production per 10(6) cells in dose of 1 microgram/ml. Heat produced by maximum thermogenic response to glucagon was twice as much as that to noradrenaline. Thermogenic response to noradrenaline was markedly increased in cold-acclimated brown adipocytes, while it was reduced in heat-acclimated ones. Thermogenic response to glucagon was significantly reduced in heat-acclimated brown adipocytes, while it was not affected in cold-acclimated brown adipocytes.
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PMID:Thermogenic responses of brown adipocytes to noradrenaline and glucagon in heat-acclimated and cold-acclimated rats. 54 97

Calorigenic actions of noradrenaline and glucagon on isolated epididymal fat cells from warm-acclimated controls, cold-acclimated and heat-acclimated rats were measured by the use of a twin-type conduction microcalorimeter. Both noradrenaline and glucagon stimulated heat production in isolated adipocytes maximally in doses of 1 microgram/ml and 10 microgram/ml, respectively. Maximal responsiveness of adipocytes per unit cell to noradrenaline was not influenced by cold acclimation, while it was reduced by heat and acclimation. Maximal response in total epididymal fat cells to noradrenaline was increased in cold acclimation and not changed in heat acclimation at increased numbers of adipocytes in both cold-acclimated and heat-acclimated animals. Maximal response per unit cell as well as per total epididymal fat cells to glucagon was increased in cold acclimation and reduced in heat acclimation. The present results indicate that the modified responses of target adipocytes to noradrenaline and glucagon are involved in the development of temperature acclimation.
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PMID:Calorigenic effects of noradrenaline and glucagon on white adipocytes in cold- and heat-acclimated rats. 57 51

Treatment with glucagon in addition to blood transfusion was compared with blood transfusion alone after one hour of hemorrhagic shock in the rat. In liver tissue Na+ increased and K+ decreased during haemorrhagic shock. After treatment the initial values were restored equally in both groups within ten minutes. Incubation of liver slices in cold Krebs' solution resulted in a pronounced increase in Na+ and decrease in K+, the values being partially restored to initial levels after subsequent incubation at 37 degrees. Thirty minutes after treatment the liver slices obtained from rats given glucagon showed a more normal ion composition after leaching and rewarming than slices from rats not given glucagon. ATP decreased and glucose and lactate increased in liver tissue during hemorrhagic shock. These variables were partially restored 30 minutes after treatment. No difference between the treatment groups was noted. Animals trreated with glucagon were, however, more efficient in reducing the elevated blood lactate level. The results suggest that the use of glucagon in the treatment of hemorrhagic shock might be of benefit for cellular function in the liver.
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PMID:Effect of glucagon and blood transfusion on liver metabolism in hemorrhagic shock. 62 13

Graded doses of pure ochratoxin A (0, 0.5, 1.0, 2.0, 4.0, and 8.0 microgram of toxin per g of feed) were incorporated into a commercial diet which was fed to chickens from hatching to 3 weeks of age, at which time the experiments were terminated. Liver glycogen levels were elevated significantly (P less than 0.05) by 4.0 and 8.0 microgram/g but not lower doses. Glucagon stimulation of glycogen mobilization was inhibited at the same concentrations. Histopathological examination revealed cytoplasmic but not nuclear deposits of glycogen in cells at the periphery of liver lobes. These data demonstrated that ochratoxin inhibited glycogenolysis. Impaired ability to generate glucose from glycogen could account for the increased susceptibility to cold stress previously reported to occur in ochratoxicosis. Based on present and prior observations, it seems possible that ochratoxin induces a syndrome which mimics the glycogen storage disease of type X which is caused by a deficiency in the cyclic AMP-dependent enzyme of the glycogenolytic enzymatic cascade.
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PMID:Decreased glycogen mobilization during ochratoxicosis in broiler chickens. 76 Jun 30

Extreme hyperinsulinism was observed in endotoxin-shock dogs made hyperglycemic by glucose infusion. Qualitatively (at least in terms of gel filtration characteristics), the insulin secreted under these conditions was normal. Hyperinsulinism was not observed in endotoxin-shock dogs not given glucose. Thus hyperinsulinism does not explain the hypoglycemia so frequently observed in endotoxin-treated dogs. Hyperinsulinsm could not be impaired degradation of insulin as disappearance of labeled insulin as well as cold insulin was comparable in control and endotoxin-treated animals. An adrenergic mechanism (either beta receptor stimulation or postadrenergic hyperresponsiveness of the beta cells) probably does not explain the hyperinsulinism observed in endotoxin-shock dogs given glucose as beta blockade failed to inhibit the hyperinsulinsm. Hyperinsulinism was not observed in endotoxin-shock dogs given tolbuamide. A tenfold rise in plasma IRG was observed in endotoxin-treated dogs whether glucose was infused or not. The persistently low IRI levels in endotoxin-treated dogs not given glucose suggest that hyperresponsiveness of the beta cell to glucagon was not present in these animals. Extreme hyperinsulinsm in response to induced hyperglycemia in endotoxin-shock dogs is unexplained. Hyperresponsiveness of the beta cell to glucose during endotoxin shock seems likely.
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PMID:Hyperinsulinism in endotoxin shock dogs. 77 54

The effects of glucagon injection on temperature regulation and some metabolic parameters were studied in the pigeon. Glucagon (100 microng/kg) always inhibited shivering and caused a fall in the oxygen consumption and body temperature of the unanesthetized pigeon at + 6 degrees C. At + 34 degrees C, the same dose of glucagon had no effect on these parameters. At 22 degrees C, glucagon produced an elevation in plasma free fatty acid (FFA) and blood glucose levels. The rise in FFA at 22 degrees C coincided with the suppression of shivering at 6 degrees C. The glucagon-mediated rise in plasma FFA, but not glucose level, was potentiated by cold ambient temperature. Adrenergic blocking agents given prior to glucagon did not abolish its effects. Phentolamine even prolonged the absence and accelerated the suppression of shivering. A dissociation in the mechanisms by which catecholamines and glucagon suppress shivering is suggested. Although mobilizing energy reserves, glucagon does not seem to be calorigenic in the pigeon at this dose. The interpretation of the changes in plasma FFA levels is discussed in relation to fuel consumption during shivering.
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PMID:Effect of glucagon on thermogenesis in the pigeon. 86 Jul 58

Glucagon infusion at a rate of 2 microgram/min for 30 min into warm-acclimated rats induced a marked rise of glucose concentration in venous blood both in the external jugular vein and in Sulzer's vein from the interscapular brown adipose tissue. In cold-acclimated rats the increase in the concentration of glucose was significantly reduced in the former vein and abolished in the latter one. These results suggest an enhanced use of glucose in the brown adipose tissue in cold-acclimated animals under the influence of glucagon.
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PMID:Reduced hyperglycemic action of glucagon in cold-acclimated rats, especially in venous drainage from brown adipose tissue. 90 68


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