Cinnamon polysaccharides reshape gut microbiota and enrich Alloprevotella rava to promote acetate-dependent choline metabolism and delay mammary aging

BACKGROUND: Aging disrupts choline metabolism, impairs mitochondrial function, and accelerates tissue degeneration. As gut microbes critically influence host nutrient handling, microbiota-targeted interventions may provide a promising strategy to delay mammary senescence. PURPOSE: This study aimed to determine whether cinnamon polysaccharides (CP) and the commensal bacterium, Alloprevotella rava, could remodel host gut microbiota, enhance host choline utilisation, improve mitochondrial function, and thereby delay mammary senescence. STUDY DESIGN: An experimental study was conducted using mouse models, maternal intervention experiments, microbiota and metabolite analyses, and complementary cellular assays to evaluate the effects of CP and A. rava on choline metabolism, mitochondrial function, mammary senescence, and offspring development. METHODS: Mice were treated with CP to assess its effects on mammary senescence and gut microbiota composition. The enrichment and supplementation of A. rava were further examined for their capacity to regulate serum and mammary choline levels, as well as the expression of host choline transporters, phosphatidylcholine biosynthetic enzymes, and microbial choline-trimethylamine (TMA) lyases (cutA and cutC). Cell-based experiments were performed to evaluate the direct effects of A. rava culture supernatant on epithelial choline uptake and biosynthesis. Metabolite analyses were used to identify the major microbial effector involved, and maternal intervention studies were conducted to assess systemic and offspring-related outcomes. RESULTS: CP alleviated mammary senescence in mice by reshaping the gut microbiota and enriching A. rava. Supplementation with A. rava increased choline levels in serum and mammary tissue, upregulated the expression of host choline transporters and phosphatidylcholine biosynthetic enzymes, and reduced microbial choline-TMA lyase expression, thereby improving host choline utilisation. The A. rava culture supernatant directly stimulated epithelial choline uptake and biosynthesis, and metabolite analyses identified acetate, rather than succinate, as the principal effector. These alterations reinforced choline-dependent phospholipid synthesis, improved mitochondrial function, and protected against cellular aging. In addition, cellular assays and maternal intervention experiments showed that A. rava enhanced epithelial metabolic resilience and supported offspring brain development. CONCLUSION: Supplementation with A. rava establishes a gut-mammary axis that promotes choline metabolism, strengthens mitochondrial function, and delays mammary senescence. Targeting specific gut microbes or their acetate-driven metabolites may represent a feasible strategy to improve maternal tissue health and support progeny neurodevelopment.