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肌肉可塑性与β₂ - 肾上腺素能受体:β₂ - 肾上腺素能受体表达对肌肉肥大和萎缩的适应性反应。

Muscle plasticity and β₂-adrenergic receptors: adaptive responses of β₂-adrenergic receptor expression to muscle hypertrophy and atrophy.

作者信息

Sato Shogo, Shirato Ken, Tachiyashiki Kaoru, Imaizumi Kazuhiko

机构信息

Laboratory of Physiological Sciences, Faculty of Human Sciences, Waseda University, 2-579-15 Mikajima, Tokorozawa, Saitama 359-1192, Japan.

出版信息

J Biomed Biotechnol. 2011;2011:729598. doi: 10.1155/2011/729598. Epub 2011 Nov 15.

Abstract

We discuss the functional roles of β₂-adrenergic receptors in skeletal muscle hypertrophy and atrophy as well as the adaptive responses of β₂-adrenergic receptor expression to anabolic and catabolic conditions. β₂-Adrenergic receptor stimulation using anabolic drugs increases muscle mass by promoting muscle protein synthesis and/or attenuating protein degradation. These effects are prevented by the downregulation of the receptor. Endurance training improves oxidative performance partly by increasing β₂-adrenergic receptor density in exercise-recruited slow-twitch muscles. However, excessive stimulation of β₂-adrenergic receptors negates their beneficial effects. Although the preventive effects of β₂-adrenergic receptor stimulation on atrophy induced by muscle disuse and catabolic hormones or drugs are observed, these catabolic conditions decrease β₂-adrenergic receptor expression in slow-twitch muscles. These findings present evidence against the use of β₂-adrenergic agonists in therapy for muscle wasting and weakness. Thus, β₂-adrenergic receptors in the skeletal muscles play an important physiological role in the regulation of protein and energy balance.

摘要

我们讨论了β₂-肾上腺素能受体在骨骼肌肥大和萎缩中的功能作用,以及β₂-肾上腺素能受体表达对合成代谢和分解代谢条件的适应性反应。使用合成代谢药物刺激β₂-肾上腺素能受体可通过促进肌肉蛋白质合成和/或减弱蛋白质降解来增加肌肉质量。这些作用会因受体下调而受到抑制。耐力训练部分通过增加运动募集的慢肌纤维中β₂-肾上腺素能受体密度来改善氧化能力。然而,过度刺激β₂-肾上腺素能受体则会抵消其有益作用。尽管已观察到β₂-肾上腺素能受体刺激对肌肉废用以及分解代谢激素或药物诱导的萎缩具有预防作用,但这些分解代谢条件会降低慢肌纤维中β₂-肾上腺素能受体的表达。这些发现提供了反对在治疗肌肉萎缩和无力中使用β₂-肾上腺素能激动剂的证据。因此,骨骼肌中的β₂-肾上腺素能受体在蛋白质和能量平衡调节中发挥着重要的生理作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b69d/3228688/ba7488c5fba2/JBB2011-729598.001.jpg

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