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运动减轻衰老SAMP8小鼠的骨骼肌萎缩:基于核磁共振代谢组学的代谢见解

Exercise Attenuates Skeletal Muscle Atrophy in Senescent SAMP8 Mice: Metabolic Insights from NMR-Based Metabolomics.

作者信息

Wu Wenfang, Zhang Linglin, Chen Yifen, Huang Caihua, Yang Longhe, Lin Donghai

机构信息

Key Laboratory for Chemical Biology of Fujian Province, High-Field NMR Center, College of Chemistry and Chemical Engineering, Xiamen University, Xiamen 361005, China.

Research and Communication Center of Exercise and Health, Xiamen University of Technology, Xiamen 361021, China.

出版信息

Molecules. 2025 Apr 30;30(9):2003. doi: 10.3390/molecules30092003.

DOI:10.3390/molecules30092003
PMID:40363810
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12073869/
Abstract

Age-related skeletal muscle atrophy is a major health concern in the elderly, contributing to reduced mobility, increased risk of falls, and metabolic dysfunction. The senescence-accelerated prone 8 (SAMP8) mouse model, known for its rapid aging and early cognitive decline, serves as an essential model for studying age-related muscle degeneration. While previous studies have shown that exercise attenuates muscle atrophy by promoting regeneration and improving strength, the underlying metabolic mechanisms remain poorly understood. This study used the SAMP8 model to evaluate the effects of exercise on muscle atrophy and associated metabolic changes. Our results show that exercise promoted muscle growth by reducing body weight, increasing skeletal muscle mass, and decreasing fat accumulation. Furthermore, exercise improved grip strength, muscle tone, and muscle fiber cross-sectional area, thereby preserving muscle functionality. NMR-based metabolomic analysis identified key metabolic pathways modulated by exercise, including glycine, serine, and threonine metabolism; alanine, aspartate, and glutamate metabolism; pyruvate metabolism; and taurine and hypotaurine metabolism. These findings underscore the therapeutic potential of exercise in combating age-related muscle wasting and elucidate the metabolic pathways underlying its benefits.

摘要

与年龄相关的骨骼肌萎缩是老年人主要的健康问题,会导致行动能力下降、跌倒风险增加以及代谢功能障碍。衰老加速易感性8(SAMP8)小鼠模型以其快速衰老和早期认知衰退而闻名,是研究与年龄相关的肌肉退化的重要模型。虽然先前的研究表明运动通过促进再生和提高力量来减轻肌肉萎缩,但其潜在的代谢机制仍知之甚少。本研究使用SAMP8模型来评估运动对肌肉萎缩及相关代谢变化的影响。我们的结果表明,运动通过减轻体重、增加骨骼肌质量和减少脂肪堆积来促进肌肉生长。此外,运动改善了握力、肌张力和肌纤维横截面积,从而保持了肌肉功能。基于核磁共振的代谢组学分析确定了运动调节的关键代谢途径,包括甘氨酸、丝氨酸和苏氨酸代谢;丙氨酸、天冬氨酸和谷氨酸代谢;丙酮酸代谢;以及牛磺酸和亚牛磺酸代谢。这些发现强调了运动在对抗与年龄相关的肌肉萎缩方面的治疗潜力,并阐明了其有益作用的代谢途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9faf/12073869/ac70a8b2869c/molecules-30-02003-g007.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9faf/12073869/759b5d462a5a/molecules-30-02003-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9faf/12073869/8671de28e14f/molecules-30-02003-g002.jpg
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本文引用的文献

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GSK3 coordinately regulates mitochondrial activity and nucleotide metabolism in quiescent oocytes.糖原合成酶激酶3(GSK3)协同调节静止期卵母细胞的线粒体活性和核苷酸代谢。
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Disruption of hepatic mitochondrial pyruvate and amino acid metabolism impairs gluconeogenesis and endurance exercise capacity in mice.
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