Oxidative Metabolism of Skeletal Muscle in Steroid Atrophy

Koski, Carol Lee; Rifenberick, David H.; Max, Stephen R.

doi:10.1001/archneur.1974.00490420073008

Cited by 42 publications

(18 citation statements)

References 24 publications

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“…Previous studies indicated abnormal protein catabolism/anabolism [1][2][3]. Decreased oxidative capacity is observed in mitochondria [6,7] but this mechanism is yet controversial [17,18]. The present study demonstrated that serum lactate levels during exercise were significantly elevated in corticosteroid-treated patients.…”

Section: Discussionsupporting

confidence: 46%

Chronic corticosteroid administration causes mitochondrial dysfunction in skeletal muscle

Mitsui¹,

Azuma²,

Nagasawa

et al. 2002

Journal of Neurology

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Corticosteroid myopathy is a major clinical problem in patients undergoing chronic corticosteroid treatment and shows insidious and progressive muscle atrophy in proximal limbs. Although several mechanisms underlying the pathophysiology of muscle injury have been postulated, precise pathogenesis is still not clear. We evaluated the mitochondrial functions in patients receiving corticosteroids compared with those in healthy controls or patients not receiving corticosteroids. The serum levels and total production of lactate were investigated by an aerobic exercise test using a bicycle ergometer. Mitochondrial respiratory activities and oxidative damage in biopsied skeletal muscles were also studied. The results of aerobic exercise tests revealed a significant overproduction of lactate in patients treated with corticosteroids ( p < 0.005), which was positively correlated with total corticosteroid doses administered ( p < 0.0001). In these patients, mitochondrial enzyme activity in complex I was significantly decreased ( p < 0.05) and oxidative damage of biopsied skeletal muscle was remarkable both in mitochondrial and nuclear DNAs ( p < 0.001). The results suggest that chronic corticosteroid administration induces mitochondrial dysfunction and oxidative damage in skeletal muscles, which may be the pathogenesis, at least in part, of corticosteroid-induced myopathy.

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Section: Discussionsupporting

confidence: 46%

Chronic corticosteroid administration causes mitochondrial dysfunction in skeletal muscle

Mitsui¹,

Azuma²,

Nagasawa

et al. 2002

Journal of Neurology

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“…The wet weight of both muscles decreased, when they treated the animals with dexamethasone, but the muscle noncollagen protein decreased only in the FT muscle (34). With regard to various morphological, biochemical, and functional parameters, most reports claim that glucocorticoids cause more profound changes to FT/white muscles than to ST/red ones, in rabbits (8,17,23,35,43,44) as well as in other species (14,15,22,29,30). However, the influence of glucocorticoids on different fiber types seems to be more complex, because in some studies, the ST fibers seemed to be the most affected (9,40).…”

Section: Discussionmentioning

confidence: 99%

Steroid Receptors in Two Types of Rabbit Skeletal Muscle*

Saartok¹

1984

Int J Sports Med

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Radiolabeled synthetic steroid hormones and a charcoal adsorption assay were used to identify cytosolic androgen, glucocorticoid, and estrogen receptors in skeletal muscle from rabbits. The presence of the receptors was verified by saturation analysis showing low-capacity, high-affinity binding for the steroid-receptor complexes, specific for each class of steroids. The concentration of androgen and estrogen receptors were of the same magnitude, whereas the corresponding value for the glucocorticoid receptor was about tenfold higher. Comparisons of fast-twitch (the gastrocnemius/plantaris complex) and slow-twitch (soleus) muscles revealed that the latter contained higher concentrations (expressed per g of tissue wet weight) of glucocorticoid and estrogen receptors, but not of androgen receptor. Expressed per mg of soluble protein, the slow-twitch muscle contained higher concentrations of all three receptors, but when related to the concentrations of all three receptors, but when related to the concentration of DNA, only the concentration of estrogen receptor was higher in the slow-twitch muscle. Different response of the two fiber types to direct action of steroid hormones can hence be expected. The fast-twitch muscle contained a higher concentration of soluble protein, whereas the slow-twitch muscle contained higher concentration of DNA, resulting in lower protein/DNA ratio, i.e., smaller "cell units," in the latter muscle.

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“…G LUCOCORTICOIDS cause severe atrophy of skeletal muscle (1,2). This effect can be caused experimentally in animals and is often a serious, consequence of Cushing's disease or long term glucocorticoid therapy in humans (1,3).…”

mentioning

confidence: 99%

Blockade of Glucocorticoid Receptor Binding and Inhibition of Dexamethasone-Induced Muscle Atrophy in the Rat by RU38486, a Potent Glucocorticoid Antagonist*

1986

Self Cite

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Glucocorticoid hormones cause marked muscular atrophy, the mechanism of which is unknown. We employed a potent glucocorticoid antagonist, RU38486 [11 beta-(4-dimethylaminophenyl)17 beta-hydroxy-17 alpha-(prop-1-ynyl)estra-4,9-dien-3-one], to determine whether intracellular glucocorticoid receptors are involved. RU38486 was shown to be an effective blocker of glucocorticoid receptor binding in vivo and in vitro. Furthermore, this compound significantly blocked the loss of body and muscle weight caused by injection of dexamethasone. These data indicate that intracellular glucocorticoid receptors are important in the etiology of steroid myopathy. Studies with glucocorticoid antagonists may lead to the design of specific therapeutic modalities for the treatment of both endogenously and exogenously produced steroid myopathies.

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Oxidative Metabolism of Skeletal Muscle in Steroid Atrophy

Cited by 42 publications

References 24 publications

Chronic corticosteroid administration causes mitochondrial dysfunction in skeletal muscle

Chronic corticosteroid administration causes mitochondrial dysfunction in skeletal muscle

Steroid Receptors in Two Types of Rabbit Skeletal Muscle*

Blockade of Glucocorticoid Receptor Binding and Inhibition of Dexamethasone-Induced Muscle Atrophy in the Rat by RU38486, a Potent Glucocorticoid Antagonist*

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