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减少的尿毒症代谢物是肌肉减少症的突出特征,与脆弱的抗氧化标记物不同。

Reduced uremic metabolites are prominent feature of sarcopenia, distinct from antioxidative markers for frailty.

机构信息

Geriatric Unit, Graduate School of Medicine, Kyoto University, Kyoto, Japan.

G0 Cell Unit, Okinawa Institute of Science and Technology Graduate University (OIST), Okinawa, Japan.

出版信息

Aging (Albany NY). 2021 Sep 7;13(17):20915-20934. doi: 10.18632/aging.203498.

DOI:10.18632/aging.203498
PMID:34492634
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8457568/
Abstract

Due to global aging, frailty and sarcopenia are increasing. Sarcopenia is defined as loss of volume and strength of skeletal muscle in elderlies, while frailty involves multiple domains of aging-related dysfunction, impaired cognition, hypomobility, and decreased social activity. However, little is known about the metabolic basis of sarcopenia, either shared with or discrete from frailty. Here we analyzed comprehensive metabolomic data of human blood in relation to sarcopenia, previously collected from 19 elderly participants in our frailty study. Among 131 metabolites, we identified 22 sarcopenia markers, distinct from 15 frailty markers, mainly including antioxidants, although sarcopenia overlaps clinically with physical frailty. Notably, 21 metabolites that decline in sarcopenia or low SMI are uremic compounds that increase in kidney dysfunction. These comprise TCA cycle, urea cycle, nitrogen, and methylated metabolites. Sarcopenia markers imply a close link between muscle and kidney function, while frailty markers define a state vulnerable to oxidative stress.

摘要

由于全球人口老龄化,衰弱和肌肉减少症的发病率正在上升。肌肉减少症是指老年人骨骼肌体积和力量的丧失,而衰弱则涉及与衰老相关的多种功能障碍、认知障碍、活动减少和社交活动减少。然而,对于肌肉减少症的代谢基础,无论是与衰弱共享还是独立于衰弱,人们知之甚少。在这里,我们分析了先前从我们的衰弱研究中收集的 19 名老年参与者的人类血液的综合代谢组学数据与肌肉减少症的关系。在 131 种代谢物中,我们确定了 22 种肌肉减少症标志物,与 15 种衰弱标志物不同,主要包括抗氧化剂,尽管肌肉减少症在临床上与身体衰弱重叠。值得注意的是,在肌肉减少症或低 SMI 中下降的 21 种代谢物是肾功能障碍时增加的尿毒症化合物。这些包括 TCA 循环、尿素循环、氮和甲基化代谢物。肌肉减少症标志物暗示肌肉和肾脏功能之间存在密切联系,而衰弱标志物则定义了一种易受氧化应激影响的状态。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3517/8457568/2f9831ebb0e5/aging-13-203498-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3517/8457568/9fe8b745ef81/aging-13-203498-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3517/8457568/daca2ca96ca5/aging-13-203498-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3517/8457568/eedba551afe7/aging-13-203498-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3517/8457568/d65c22b5aaae/aging-13-203498-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3517/8457568/2f9831ebb0e5/aging-13-203498-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3517/8457568/9fe8b745ef81/aging-13-203498-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3517/8457568/daca2ca96ca5/aging-13-203498-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3517/8457568/eedba551afe7/aging-13-203498-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3517/8457568/d65c22b5aaae/aging-13-203498-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3517/8457568/2f9831ebb0e5/aging-13-203498-g005.jpg

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