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Evaluation of the endogenous glucocorticoid hypothesis of denervation atrophy
Abstract:
We studied the effects of oral administration of RU38486, a potent and selective glucocorticoid antagonist, on muscle weight, non-collagen protein content, and selected enzyme activities (choline acetyltransferase, glucose-6-phosphate dehydrogenase, and glutamine synthetase) following denervation of rat skeletal muscle. Neither decreases in muscle weight, protein content, and choline acetyltransferase activity, nor increases in the activities of glucose-6-phosphate dehydrogenase and glutamine synthetase were affected by RU38486. These data do not support the hypothesis that denervation atrophy results from enhanced sensitivity of muscle to endogenous glucocorticoids.
Insights
This study found that RU38486, a glucocorticoid antagonist, did not alter muscle changes after denervation in rats. Therefore, enhanced sensitivity to glucocorticoids does not cause denervation atrophy.
Area of Science:
- Muscle physiology
- Endocrinology
- Neuroscience
Background:
- Skeletal muscle denervation leads to atrophy.
- Glucocorticoids are implicated in muscle wasting.
- RU38486 is a selective glucocorticoid receptor antagonist.
Purpose of the Study:
- To investigate the role of glucocorticoids in denervation-induced skeletal muscle atrophy.
- To determine if blocking glucocorticoid receptors with RU38486 affects muscle wasting parameters.
Main Methods:
- Oral administration of RU38486 to rats.
- Skeletal muscle denervation was performed.
- Measurements included muscle weight, non-collagen protein content, and enzyme activities (choline acetyltransferase, glucose-6-phosphate dehydrogenase, glutamine synthetase).
Main Results:
- RU38486 did not affect the decrease in muscle weight or protein content.
- RU38486 did not alter choline acetyltransferase activity.
- RU38486 did not affect the increase in glucose-6-phosphate dehydrogenase and glutamine synthetase activities.
Conclusions:
- The findings do not support the hypothesis that denervation atrophy is caused by increased muscle sensitivity to endogenous glucocorticoids.
- Glucocorticoid antagonism does not prevent or modify the atrophic changes in skeletal muscle following denervation.