Evaluation of the endogenous glucocorticoid hypothesis of denervation atrophy.
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.
D000818:Animals; D002795:Choline O-Acetyltransferase / Q000378:metabolism; D004963:Estrenes / Q000494:pharmacology; D005938:Glucocorticoids / Q000502:physiology*; D005954:Glucosephosphate Dehydrogenase / Q000378:metabolism; D005974:Glutamate-Ammonia Ligase / Q000378:metabolism; D008297:Male; D015735:Mifepristone; D009121:Muscle Denervation; D009132:Muscles / Q000201:enzymology / Q000473:pathology; D009133:Muscular Atrophy / Q000201:enzymology / Q000503:physiopathology*; D009929:Organ Size; D051381:Rats
D004963:Estrenes; D005938:Glucocorticoids; D015735:Mifepristone; D005954:Glucosephosphate Dehydrogenase; D002795:Choline O-Acetyltransferase; D005974:Glutamate-Ammonia Ligase