Elucidating the underlying mechanism of amino acids to regulate muscle protein synthesis: Effect on human health

氨基酸 mTORC1型 蛋白质分解代谢 生物化学 蛋白质生物合成 分解代谢 生物 蛋白质降解 化学 新陈代谢 PI3K/AKT/mTOR通路 信号转导
作者
Xiaokang Lv,Chuanshe Zhou,Qiongxian Yan,Zhiliang Tan,Jinhe Kang,Shaoxun Tang
出处
期刊:Nutrition [Elsevier BV]
卷期号:103-104: 111797-111797 被引量:35
标识
DOI:10.1016/j.nut.2022.111797
摘要

Maintaining muscle quality throughout life is crucial to human health and well-being. Muscle is the most extensive form of protein storage in the human body; skeletal muscle mass is determined by the balance between muscle protein synthesis (MPS) and muscle protein breakdown (MPB). MPB provides amino acids needed by various organs; however, excessive MPB, especially with aging, may cause loss of muscle mass and a decline in motor function, even threatening life. The turnover of muscle protein is vital to the health of humans. Thus, although the study of MPS and MPB has theoretical and practical significance, the network that controls MPS is very complicated and we cannot discuss both MPS and MPB in a single review. Therefore, the aim of this review is to discuss the regulation of MPS, especially by amino acids. Amino acids regulate protein synthesis in cell and animal models, but compelling evidence for amino acids promoting protein synthesis in human muscles is ambiguous. Studies on the stimulation of human MPS by branched-chain amino acids (BCAAs) have been inconsistent. Amino acids other than BCAAs such as threonine and tryptophan may also have MPS-stimulating effects, and alternatives to BCAAs, such as β-hydroxy-β-methyl butyrate and branched-chain keto acids are also worthy of further investigation. Amino acids coordinate protein synthesis and degradation through the mechanistic target of rapamycin complex 1 (mTORC1); however, the amino acid-mTORC1-protein synthesis pathway is complex, and new insights into amino acid control continue to emerge. Understanding how amino acids control MPS is of forward-looking significance for treating muscle mass loss during human aging.
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