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富含L-色氨酸的饮食通过代谢物吲哚-3-乙酸和芳烃受体激活减轻高强度运动诱导的肝功能障碍。

L-Tryptophan-Rich Diet Alleviates High-Intensity-Exercise-Induced Liver Dysfunction via the Metabolite Indole-3-Acetic Acid and AhR Activation.

作者信息

Wang Dawei, Hou Pengfei, Lang Hedong, Xia Yundong, Bai Qian, Yao Yu, Yi Long, Mi Mantian

机构信息

Research Center for Nutrition and Food Safety, Chongqing Key Laboratory of Nutrition and Health, Chongqing Medical Nutrition Research Center, Institute of Military Preventive Medicine, Third Military Medical University, Chongqing 400038, China.

出版信息

Cells. 2025 Apr 16;14(8):605. doi: 10.3390/cells14080605.

DOI:10.3390/cells14080605
PMID:40277929
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12026455/
Abstract

High-intensity exercise (HIE) induces liver dysfunction and is detrimental to exercise performance. The underlying mechanism and preventive strategy urgently need to be explored. We increased the amount of tryptophan appropriately in the diet and explored the effect of an L-tryptophan-rich diet on the alleviation of HIE-induced liver dysfunction and the underlying mechanism. In this work, by establishing a C57BL/6 mouse model of high-intensity swimming exercise, the results demonstrated an L-tryptophan-rich diet significantly attenuated HIE-induced liver dysfunction, which was associated with increased levels of the tryptophan metabolite indole-3-acetic acid (IAA). Furthermore, IAA indeed exerted a protective effect against HIE-induced liver dysfunction in vivo and LPS-induced hepatocyte dysfunction in vitro. In conclusion, an L-tryptophan-rich diet may be a promising strategy to prevent HIE-induced liver dysfunction and metabolic disturbance via the metabolite indole-3-acetic acid and AhR activation.

摘要

高强度运动(HIE)会导致肝功能障碍,并对运动表现产生不利影响。其潜在机制和预防策略亟待探索。我们在饮食中适当增加色氨酸的量,并探讨富含L-色氨酸的饮食对减轻HIE诱导的肝功能障碍及其潜在机制的影响。在这项工作中,通过建立高强度游泳运动的C57BL/6小鼠模型,结果表明富含L-色氨酸的饮食显著减轻了HIE诱导的肝功能障碍,这与色氨酸代谢产物吲哚-3-乙酸(IAA)水平的升高有关。此外,IAA确实在体内对HIE诱导的肝功能障碍以及在体外对脂多糖诱导的肝细胞功能障碍发挥了保护作用。总之,富含L-色氨酸的饮食可能是一种有前景的策略,可通过代谢产物吲哚-3-乙酸和芳烃受体(AhR)激活来预防HIE诱导的肝功能障碍和代谢紊乱。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a09/12026455/9997dc24b409/cells-14-00605-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a09/12026455/2f4409a2f00e/cells-14-00605-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a09/12026455/751c0a8f795d/cells-14-00605-g002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a09/12026455/843e5f8dd881/cells-14-00605-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a09/12026455/c4df2df8ade1/cells-14-00605-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a09/12026455/9997dc24b409/cells-14-00605-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a09/12026455/2f4409a2f00e/cells-14-00605-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a09/12026455/751c0a8f795d/cells-14-00605-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a09/12026455/f06d4680c6a4/cells-14-00605-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a09/12026455/a0a471d1345d/cells-14-00605-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a09/12026455/843e5f8dd881/cells-14-00605-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a09/12026455/c4df2df8ade1/cells-14-00605-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a09/12026455/9997dc24b409/cells-14-00605-g007.jpg

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本文引用的文献

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Gut Microbes. 2024 Jan-Dec;16(1):2377576. doi: 10.1080/19490976.2024.2377576. Epub 2024 Jul 27.
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Cryo-EM structure of the cytosolic AhR complex.胞质芳烃受体复合物的冷冻电镜结构
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Dihydromyricetin-Encapsulated Liposomes Inhibit Exhaustive Exercise-Induced Liver Inflammation by Orchestrating M1/M2 Macrophage Polarization.
二氢杨梅素包封脂质体通过调控M1/M2巨噬细胞极化抑制力竭运动诱导的肝脏炎症
Front Pharmacol. 2022 Jun 2;13:887263. doi: 10.3389/fphar.2022.887263. eCollection 2022.
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Dihydromyricetin ameliorates liver fibrosis via inhibition of hepatic stellate cells by inducing autophagy and natural killer cell-mediated killing effect.二氢杨梅素通过诱导自噬和自然杀伤细胞介导的杀伤作用抑制肝星状细胞,从而改善肝纤维化。
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The Acute Effects of Swimming Exercise on PGC-1α-FNDC5/Irisin-UCP1 Expression in Male C57BL/6J Mice.游泳运动对雄性C57BL/6J小鼠PGC-1α-FNDC5/鸢尾素-UCP1表达的急性影响
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Nutrients. 2019 Sep 3;11(9):2062. doi: 10.3390/nu11092062.