Effect of Gut Microbiota-Mediated Tryptophan Metabolism on Inflammaging in Frailty and Sarcopenia

Author:

Xu YuShuang1,Mao Tao1,Wang YouJun2,Qi XingSi1,Zhao WenJun1,Chen Hao1,Zhang CuiPing1,Li XiaoYu1

Affiliation:

1. Department of Gastroenterology, Affiliated Hospital of Qingdao University , Qingdao, Shandong , People’s Republic of China

2. Department of Gastroenterology, Central Hospital Affiliated to ShanDong First Medical University , Jinan , People’s Republic of China

Abstract

Abstract Frailty syndrome refers to the nonspecific state of increased body vulnerability and decreased antistress and recovery abilities after stress during aging. Sarcopenia is the major component of frailty and is characterized by the gradual loss of muscle mass, strength, and function with age. Inflammaging is the gradual increase in inflammatory status during aging, and it disrupts immune tolerance, causes physiological changes in tissues, organs, and normal cells, and is related to frailty and sarcopenia. The gut microbiota is an extremely complex and diverse microbial community that coevolves with the host. The composition and structure of the gut microbiota and the metabolism of tryptophan (Trp) significantly change in older adults with frailty and sarcopenia. The gut microbiota participates in regulating the Trp metabolic pathways of kynurenine (Kyn), 5-hydroxytryptamine (5-HT), and indole in the gastrointestinal tract. The Trp metabolites derived from the gut microbiota may synergistically promote the occurrence of age-related frailty and sarcopenia by promoting inflammation in the intestines, nervous system, and muscles. The role and mechanisms of the gut microbiota, Trp metabolism, and inflammaging in age-related frailty and sarcopenia may be a worthwhile research direction to help promote healthy aging.

Funder

National Natural Science Foundation of China

Taishan Young Scholars Program of Shandong Province

2023 Qingdao Technology Benefiting Demonstration Project

Qingdao Chinese Medicine Technology Project

Publisher

Oxford University Press (OUP)

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