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Branched-chain amino acid supplementation ameliorates angiotensin II-induced skeletal muscle atrophy.
Life Sciences ( IF 6.1 ) Pub Date : 2020-03-28 , DOI: 10.1016/j.lfs.2020.117593
Katsuma Yamanashi 1 , Shintaro Kinugawa 1 , Arata Fukushima 1 , Naoya Kakutani 2 , Shingo Takada 3 , Yoshikuni Obata 1 , Ippei Nakano 1 , Takashi Yokota 1 , Yasuyuki Kitaura 4 , Yoshiharu Shimomura 4 , Toshihisa Anzai 1
Affiliation  

AIMS Sarcopenia is characterized by muscle mass and strength loss and reduced physical activity. Branched-chain amino acids (BCAAs) were recently described as an activator of protein synthesis via mammalian target of rapamycin (mTOR) signaling for muscle atrophy. In cardiovascular diseases, excessive activation of the renin-angiotensin system may induce an imbalance of protein synthesis and degradation, and this plays a crucial role in muscle atrophy. We investigated the effects of BCAAs on angiotensin II (Ang II)-induced muscle atrophy in mice. MATERIALS AND METHODS We administered Ang II (1000 ng/kg/min) or vehicle to 10-12-week-old male C57BL/6J mice via subcutaneous osmotic minipumps for 4 weeks with or without BCAA supplementation (3% BCAA in tap water). KEY FINDINGS The skeletal muscle weight/tibial length and cross-sectional area were smaller in the Ang II mice than the vehicle mice; these changes were induced by an imbalance of protein synthesis and degradation signaling such as Akt/mTOR and MuRF-1/Atrogin-1. Compared to the Ang II mice, the mTOR signaling was significantly activated and Ang II-induced muscle atrophy was ameliorated in the Ang II + BCAA mice, and this attenuated the reduction of exercise capacity. Notably, the decrease of muscle weight/tibial length in the fast-twitch dominant muscles (e.g., the extensor digitorum longus) was significantly ameliorated compared to that in the slow-twitch dominant muscles (e.g., soleus). Histologically, the effect of BCAA was larger in fast-twitch than slow-twitch fibers, which may be related to the difference in BCAA catabolism. SIGNIFICANCE BCAA supplementation could contribute to the prevention of skeletal muscle atrophy induced by Ang II.

中文翻译:

支链氨基酸补充改善了血管紧张素II诱导的骨骼肌萎缩。

AIMS肌肉减少症的特征在于肌肉质量和力量下降以及体育活动减少。支链氨基酸(BCAAs)最近被描述为通过哺乳动物雷帕霉素靶标(mTOR)信号指示肌肉萎缩的蛋白质合成激活剂。在心血管疾病中,肾素-血管紧张素系统的过度激活可能导致蛋白质合成和降解失衡,这在肌肉萎缩中起关键作用。我们调查了BCAAs对血管紧张素II(Ang II)诱导的小鼠肌肉萎缩的影响。材料和方法我们通过皮下渗透微型泵对10-12周龄的雄性C57BL / 6J小鼠施用Ang II(1000 ng / kg / min)或赋形剂,持续4周,添加或不添加BCAA(自来水中3%BCAA) 。主要发现Ang II小鼠的骨骼肌重量/胫骨长度和横截面积比媒介物小鼠小。这些变化是由蛋白质合成和降解信号如Akt / mTOR和MuRF-1 / Atrogin-1的失衡引起的。与Ang II小鼠相比,在Ang II + BCAA小鼠中mTOR信号被显着激活,并且Ang II诱导的肌肉萎缩得到改善,这减弱了运动能力的降低。值得注意的是,与缓慢抽搐的优势肌肉(例如,比目鱼)相比,快速抽搐的优势肌肉(例如,趾长伸肌)的肌肉重量/胫骨长度的减少得到了明显改善。从组织学上讲,快支纤维的BCAA效果要好于慢支纤维,这可能与BCAA分解代谢的差异有关。
更新日期:2020-03-28
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