Bifidobacterium adolescentis-derived nicotinic acid improves host skeletal muscle mitochondrial function to ameliorate sarcopenia
QH301-705.5
CP: Microbiology
Biology (General)
CP: Metabolism
DOI:
10.1016/j.celrep.2025.115265
Publication Date:
2025-02-04T19:04:49Z
AUTHORS (8)
ABSTRACT
Sarcopenia significantly diminishes quality of life and increases mortality risk in older adults. While the connection between gut microbiome muscle health is recognized, underlying mechanisms are poorly understood. In this study, shotgun metagenomics revealed that Bifidobacterium adolescentis notably depleted individuals with sarcopenia, correlating reduced mass function. This finding was validated aged mice. Metabolomics analysis identified nicotinic acid as a key metabolite produced by B. adolescentis, linked to improvements functionality sarcopenia. Mechanistically, restores nicotinamide adenine dinucleotide (NAD+) levels muscle, inhibits FoxO3/Atrogin-1/Murf-1 axis, promotes satellite cell proliferation, reducing atrophy. Additionally, NAD+ activation enhances silent-information-regulator 1 (SIRT1)/peroxisome-proliferator-activated-receptor-γ-coactivator 1-alpha (PGC-1α) stimulating mitochondrial biogenesis promoting oxidative metabolism slow-twitch fibers, ultimately improving Our findings suggest adolescentis-derived could be promising therapeutic strategy for
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