Glucocorticoids and Skeletal Muscle

Glucocorticoids and Skeletal Muscle
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DOI:
10.1007/978-1-4939-2895-8_7
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发表时间:
2015-01-01
期刊:
GLUCOCORTICOID SIGNALING: FROM MOLECULES TO MICE TO MAN
影响因子:
--
通讯作者:
Furlow, J. David
Furlow, J. David
中科院分区:
其他
文献类型:
--
作者:
Bodine, Sue C.;Furlow, J. David

文献摘要

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已知糖皮质激素可调节骨骼肌中的蛋白质代谢,产生与胰岛素相反的分解代谢作用。在许多分解代谢疾病中,例如败血症、饥饿和癌症恶病质,内源性糖皮质激素升高,导致肌肉质量和功能丧失。此外,经常急性和长期给予外源性糖皮质激素来治疗炎症,例如哮喘、慢性阻塞性肺病和类风湿性关节炎,导致肌肉萎缩。本章将详细介绍糖皮质激素引起的肌肉萎缩的性质,并讨论糖皮质激素对肌肉分解代谢作用的机制。
Glucocorticoids are known to regulate protein metabolism in skeletal muscle, producing a catabolic effect that is opposite that of insulin. In many catabolic diseases, such as sepsis, starvation, and cancer cachexia, endogenous glucocorticoids are elevated contributing to the loss of muscle mass and function. Further, exogenous glucocorticoids are often given acutely and chronically to treat inflammatory conditions such as asthma, chronic obstructive pulmonary disease, and rheumatoid arthritis, resulting in muscle atrophy. This chapter will detail the nature of glucocorticoid-induced muscle atrophy and discuss the mechanisms thought to be responsible for the catabolic effects of glucocorticoids on muscle.