Adaptive responses of rats to prolonged treatment with epinephrine

1981 ◽  
Vol 241 (1) ◽  
pp. C55-C58 ◽  
Author(s):  
R. D. Fell ◽  
S. E. Terblanche ◽  
W. W. Winder ◽  
J. O. Holloszy
Keyword(s):  
Blood Glucose ◽  
Exercise Training ◽  
Muscle Glycogen ◽  
Plasma Insulin ◽  
Citrate Synthase ◽  
Liver Glycogen ◽  
Prolonged Treatment ◽  
Daily Injection ◽  
Adaptive Responses ◽  
Response To Exercise

Rats were given a daily injection of L-epinephrine, 100 micrograms/100 g body wt, for 6 wk. The hearts of the epinephrine-treated animals were heavier (11.5%), and blood glucose and plasma insulin concentrations were lower than those of control rats. Acute responses to epinephrine were compared in the two groups. An increase in blood glucose and decreases in plasma insulin, liver glycogen, and muscle glycogen occurred in both groups. The magnitude of these responses were similar in the two groups except for the decrease in muscle glycogen, which was smaller in the chronic epinephrine-treatment group. There were no changes in respiratory capacity, citrate synthase or succinate dehydrogenase activities, or in cytochrome c concentration in skeletal muscle in response to 6 wk of epinephrine treatment. These results are compatible with the suggestion that catecholamines may play a role in some of the metabolic and cardiac adaptations to exercise training. However, they argue strongly against the hypothesis that catecholamines are responsible for inducing the increase in muscle mitochondria that occurs in response to exercise training.

High E/e′ disrupts the rapid lowering of blood glucose in response to exercise training

2012 ◽  
Vol 10 (4) ◽  
pp. 119-124
Author(s):  
Yamato Fukuda ◽  
Kumiko Yoshimura ◽  
Yoshiharu Fukuda ◽  
Nobuo Fukuda
Keyword(s):  
Blood Glucose ◽  
Exercise Training ◽  
Response To Exercise

Effects of exercise training on glucose transport and cell surface GLUT-4 in isolated rat epitrochlearis muscle

1997 ◽  
Vol 272 (2) ◽  
pp. E320-E325 ◽  
Author(s):  
T. H. Reynolds ◽  
J. T. Brozinick ◽  
M. A. Rogers ◽  
S. W. Cushman
Keyword(s):  
Exercise Training ◽  
Cell Surface ◽  
Glucose Transport ◽  
Muscle Glycogen ◽  
Citrate Synthase ◽  
Transport Activity ◽  
Glut 4 ◽  
Isolated Rat

The effects of exercise training on maximal glucose transport activity and cell surface GLUT-4 were examined in rat epitrochlearis muscle. Five days of swim training (2 x 3 h/day) produce a significant increase in citrate synthase activity (24.5 +/- 0.6 vs. 20.1 +/- 0.7 micromol x min(-1) x g(-1)), GLUT-4 content (22.9 +/- 0.8 vs. 17.4 +/- 0.4% GLUT-4 standard), and glycogen levels (54.3 +/- 9.4 vs. 28.6 +/- 9.4 micromol/g). Maximally, insulin-stimulated glucose transport activity and cell surface GLUT-4 are increased by 55 (1.50 +/- 0.11 vs. 0.97 +/- 0.10 micromol x ml(-1) x 20 min(-1)) and 48% [12.0 +/- 0.8 vs. 8.1 +/- 0.9 disintegrations x min(-1) (dpm) x mg(-1)], respectively, in exercise-trained epitrochlearis muscles. In contrast, hypoxia-stimulated glucose transport activity and cell surface GLUT-4 are reduced by 38 (0.78 +/- 0.08 vs.1.25 +/- 0.14 micromol x ml(-1) x 20 min(-1)) and 40% (5.7 +/- 0.9 vs. 9.4 +/- 1.2 dpm/mg), respectively, in exercise-trained epitrochlearis muscles. These results demonstrate that changes in insulin- and hypoxia-stimulated glucose transport activity after exercise training are fully accounted for by the appearance of cell surface GLUT-4 and support the concept of two intracellular pools of GLUT-4. Finally, we propose that high levels of muscle glycogen with exercise training may contribute to the decrease in hypoxia-stimulated glucose transport activity.

Some Effects of Metabolic Acidosis on Carbohydrate Metabolism in the Rat

1970 ◽  
Vol 39 (3) ◽  
pp. 375-382 ◽  
Author(s):  
G. A. O. Alleyne ◽  
H. S. Fraser ◽  
H. S. Besterman
Keyword(s):  
Metabolic Acidosis ◽  
Blood Glucose ◽  
Muscle Glycogen ◽  
Fasting Blood Glucose ◽  
Liver Glycogen ◽  
Carbohydrate Diet ◽  
And Control ◽  
Peak Blood ◽  
Peak Blood Glucose

1. Metabolic acidosis was induced by feeding ammonium chloride to rats which were maintained on a carbohydrate diet for 48 h. 2. Fasting blood glucose was the same in acidotic and control animals, but there was an increase in liver glycogen in the former. Muscle glycogen was unchanged. 3. In vitro glycogenolysis was the same in liver slices from normal rats when incubated at a range of pH from 6·90 to 7·40. 4. The peak blood glucose in response to intraperitoneal injections of glucagon was the same in control and acidotic rats. The rate of disappearance of glucose was slower in acidotic rats both after the glucagon induced hyperglycaemia and after intravenously injected glucose. 5. Liver phosphorylase, total glycogen synthetase and the I form of this enzyme were unchanged in acidosis. 6. The data are compatible with the hypothesis that in the acidotic rat there is a block in glycolysis—possibly at the phosphofructokinase step.

Adaptations of skeletal muscle to endurance exercise and their metabolic consequences

1984 ◽  
Vol 56 (4) ◽  
pp. 831-838 ◽  
Author(s):  
J. O. Holloszy ◽  
E. F. Coyle
Keyword(s):  
Skeletal Muscle ◽  
Blood Glucose ◽  
Exercise Training ◽  
Endurance Exercise ◽  
Muscle Glycogen ◽  
Lactate Production ◽  
Strenuous Exercise ◽  
Mitochondrial Content ◽  
Respiratory Capacity ◽  
Endurance Exercise Training

Regularly performed endurance exercise induces major adaptations in skeletal muscle. These include increases in the mitochondrial content and respiratory capacity of the muscle fibers. As a consequence of the increase in mitochondria, exercise of the same intensity results in a disturbance in homeostasis that is smaller in trained than in untrained muscles. The major metabolic consequences of the adaptations of muscle to endurance exercise are a slower utilization of muscle glycogen and blood glucose, a greater reliance on fat oxidation, and less lactate production during exercise of a given intensity. These adaptations play an important role in the large increase in the ability to perform prolonged strenuous exercise that occurs in response to endurance exercise training.

scholarly journals The Role of Hormones in the Regulation of Glycogen Metabolism in the Clawed Toad Xenopus Laevis (Daudin)

2019 ◽  
pp. 17-24
Author(s):  
Daphna Atar-Zwillenberg ◽  
Michael Atar ◽  
Gianni Morson ◽  
Udo Spornitz
Keyword(s):  
Blood Glucose ◽  
Xenopus Laevis ◽  
Muscle Glycogen ◽  
Hormonal Regulation ◽  
Glycogen Content ◽  
Glycogen Metabolism ◽  
Liver Glycogen ◽  
Hepatic Glycogen ◽  
Lipid Levels ◽  
Liver Glycogen Content

The hormonal regulation of amphibian glycogen metabolism was studied in Xenopus laevis as a typical member of the anurans (tailless amphibians).The main focus of this study was given to the effects of various hormones on the glycogen/glucose balance in adult toads. We determined biochemically the liver and muscle glycogen contents as well as the blood glucose and lipid levels for a number of hormones and also diabetes inducing substances. Additionally, we examined ultrastructure changes in hepatocytes induced by the various treatments, and also investigated the activity of carbohydrate-relevant enzymes by histochemistry. With one exception, the liver glycogen content of Xenopus remained basically unchanged by the treatments or was even slightly enhanced. Only human chorionic gonadotropin, through which the vitellogenic response is triggered, prompts a significant decrease of liver glycogen in females. Under the same conditions the male liver glycogen content remained stable. Muscle glycogen contents were not affected by any of the treatments. Blood glucose and lipid levels on the other hand were elevated considerably in both sexes after application of either epinephrine or cortisol. The ultrastructural examination revealed a proliferation of Rough Endoplasmic Reticulum (RER) in hepatocytes from epinephrine treated toads of both sexes as well as from HCG treated females. By histochemistry, we detected an elevated glucose-6-phosphatase activity in the hepatocytes from toads treated with either epinephrine or cortisol. These treatments also led to enhanced glycogen phosphorylase activity in males, and to a slightly elevated glyceraldehyde-3-phosphate dehydrogenase activity in females. Our results show that the hepatic glycogen is extremely stable in adult Xenopus. Only vitellogenesis causes a marked utilization of glycogen. Since the blood glucose levels are elevated in epinephrine or cortisol treated toads without the liver glycogen being affected, we conclude that either protein and/or lipid metabolism are involved in carbohydrate metabolism in Xenopus laevis.

scholarly journals A Quantitative Trait Locus on 7q31 for the Changes in Plasma Insulin in Response to Exercise Training: The HERITAGE Family Study

Diabetes ◽  
2003 ◽  
Vol 52 (6) ◽  
pp. 1583-1587 ◽  
Author(s):  
T. A. Lakka ◽  
T. Rankinen ◽  
S. J. Weisnagel ◽  
Y. C. Chagnon ◽  
T. Rice ◽  
...  
Keyword(s):  
Quantitative Trait Locus ◽  
Exercise Training ◽  
Quantitative Trait ◽  
Plasma Insulin ◽  
Family Study ◽  
Trait Locus ◽  
Response To Exercise

Effects of fasting and insulin on carbohydrate metabolism of the domestic fowl

1959 ◽  
Vol 197 (1) ◽  
pp. 47-51 ◽  
Author(s):  
R. L. Hazelwood ◽  
F. W. Lorenz
Keyword(s):  
Growth Hormone ◽  
Body Weight ◽  
Blood Glucose ◽  
Carbohydrate Metabolism ◽  
Domestic Fowl ◽  
Liver Glycogen ◽  
Rapid Decrease ◽  
Daily Injection ◽  
Prolonged Fasting ◽  
Free Insulin

Prolonged fasting caused a rise in blood glucose which reached a maximum above the prefast level on the 6th day. Concurrently the liver glycogen, rapidly depleted at the start of the fast, was partially replaced. Blood NPN increased continuously. Thus, gluconeogenesis appeared likely not only to be responsible for the blood glucose increase but also to play a role in the restoration of liver glycogen after initial glycogenolysis due to fasting. Fasting for 48 hours increased cardiac glycogen up to three times the prefasting level; a rapid decrease in this moiety occurred with further abstinence. Glucagon and growth hormone increased the cardiac glycogen of nonfasted birds; but had little, if any, influence on the effects of fasting. The daily injection of 60–70 u of either regular or HGF-free insulin per kilogram body weight resulted in an hyperglycemic rebound 24 hours after each injection. This rebound could be blocked completely by feeding Dibenzyline.

Glycogenolytic action of mercaptoethylamine

1959 ◽  
Vol 196 (2) ◽  
pp. 261-264 ◽  
Author(s):  
Joseph E. Sokal ◽  
Edward J. Sarcione ◽  
Kornel E. Gerszi
Keyword(s):  
Blood Glucose ◽  
Muscle Glycogen ◽  
Liver Glycogen ◽  
Intragastric Administration ◽  
Rats And Mice ◽  
Higher Doses

The observation of Bacq, Herve and Fischer ( Bull. acad. roy. méd. Belg. 18: 226, 1953), that mercaptoethylamine induces depletion of liver glycogen in rats and mice, has been confirmed. The disulfide form of the drug (cystamine) is more consistent in its action than the sulfhydryl form (cysteamine). Parenteral doses of 150 mg/kg induce 70– 90% depletion of liver glycogen of fed rats in 2–3 hours. Intragastric administration is also effective, but higher doses are required. The compound is effective in adrenodemedullated and in depancreatized rats, and may, therefore, act directly on the liver. Reduction of muscle glycogen was observed in normal and depancreatized, but not in adrenodemedullated, rats. In adrenodemedullated rats, but not in normal or depancreatized rats, mercaptoethylamine induced distinct declines in blood glucose, in spite of hepatic glycogenolysis. These findings suggest that this agent stimulates the secretion of epinephrine and of insulin.

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