亮氨酸通过抑制泛素连接酶来减轻骨骼肌萎缩。

Leucine attenuates skeletal muscle wasting via inhibition of ubiquitin ligases.

机构信息

Department of Cell and Developmental Biology, Institute of Biomedical Sciences, University of São Paulo, Avenida Prof. Lineu Prestes, 1524, Butantã, CEP 05508-900, São Paulo, Brazil.

出版信息

Muscle Nerve. 2010 Jun;41(6):800-8. doi: 10.1002/mus.21578.

Abstract

The aim of this study was to assess the effect of leucine supplementation on elements of the ubiquitin-proteasome system (UPS) in rat skeletal muscle during immobilization. This effect was evaluated by submitting the animals to a leucine supplementation protocol during hindlimb immobilization, after which different parameters were determined, including: muscle mass; cross-sectional area (CSA); gene expression of E3 ligases/deubiquitinating enzymes; content of ubiquitinated proteins; and rate of protein synthesis. Our results show that leucine supplementation attenuates soleus muscle mass loss driven by immobilization. In addition, the marked decrease in the CSA in soleus muscle type I fibers, but not type II fibers, induced by immobilization was minimized by leucine feeding. Interestingly, leucine supplementation severely minimized the early transient increase in E3 ligase [muscle ring finger 1 (MuRF1) and muscle atrophy F-box (MAFbx)/atrogin-1] gene expression observed during immobilization. The reduced peak of E3 ligase gene expression was paralleled by a decreased content of ubiquitinated proteins during leucine feeding. The protein synthesis rate decreased by immobilization and was not affected by leucine supplementation. Our results strongly suggest that leucine supplementation attenuates muscle wasting induced by immobilization via minimizing gene expression of E3 ligases, which consequently could downregulate UPS-driven protein degradation. It is notable that leucine supplementation does not restore decreased protein synthesis driven by immobilization.

摘要

本研究旨在评估亮氨酸补充对制动大鼠骨骼肌泛素-蛋白酶体系统(UPS)成分的影响。通过在动物接受后肢制动期间进行亮氨酸补充方案,评估这种影响,之后确定了不同的参数,包括:肌肉质量;横截面积(CSA);E3 连接酶/去泛素化酶的基因表达;泛素化蛋白含量;以及蛋白质合成率。我们的结果表明,亮氨酸补充可减轻制动引起的比目鱼肌质量损失。此外,亮氨酸喂养可最大程度地减少制动引起的比目鱼肌 I 型纤维 CSA 的明显下降,但 II 型纤维则不会。有趣的是,亮氨酸补充严重地最小化了制动期间观察到的 E3 连接酶(肌肉环指 1(MuRF1)和肌肉萎缩 F 盒(MAFbx)/肌萎缩蛋白 1(atrogin-1))基因表达的早期短暂增加。E3 连接酶基因表达的峰值降低伴随着亮氨酸喂养期间泛素化蛋白含量的降低。制动引起的蛋白质合成率降低,但亮氨酸补充对其没有影响。我们的结果强烈表明,亮氨酸补充通过最小化 E3 连接酶的基因表达来减轻制动引起的肌肉萎缩,这可能会下调 UPS 驱动的蛋白质降解。值得注意的是,亮氨酸补充并不能恢复制动引起的蛋白质合成减少。

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