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DOI 10.1093/gerona/glae044

Медицинская библиотека · The journals of gerontology. Series A, Biological sciences and medical sciences · 2024

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

Xu YuShuang, Mao Tao, Wang YouJun, Qi XingSi, Zhao WenJun, Chen Hao, Zhang CuiPing, Li XiaoYu

СтатьяОбзорПоддержка исследования: вне правительства СШАПеревод в очереди

Аннотация

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.

Для цитирования: Xu YuShuang, Mao Tao, Wang YouJun, Qi XingSi, Zhao WenJun, Chen Hao, Zhang CuiPing, Li XiaoYu. Effect of Gut Microbiota-Mediated Tryptophan Metabolism on Inflammaging in Frailty and Sarcopenia.. The journals of gerontology. Series A, Biological sciences and medical sciences. 2024. DOI: 10.1093/gerona/glae044.

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