Deoxycholic acid ameliorates postmenopausal osteoporosis by rebalancing BMSC differentiation and suppressing NF-κB signaling.

Early human evidence such as case series or small samples is exploring possible benefits.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Postmenopausal osteoporosis (PMOP) represents a significant global health issue associated with aging, primarily driven by estrogen deficiency. Although the gut-bone axis has garnered increasing attention, the specific bioactive metabolites and molecular mechanisms linking gut dysbiosis to bone loss remain to be fully elucidated. In this study, we investigated the gut-bile acid-bone axis by integrating clinical data with mechanistic studies in an ovariectomized mouse model. Clinically, serum total bile acid levels were positively correlated with bone mineral density in PMOP patients. In ovariectomized mice, estrogen withdrawal induced alterations in the abundance of gut microbiota involved in secondary bile acid biosynthesis, including Clostridium, Bifidobacterium, and Bacteroides, resulting in decreased serum deoxycholic acid (DCA) levels. Notably, Mendelian randomization analysis provided genetic evidence supporting a causal relationship between serum DCA levels and lumbar spine bone mineral density. Therapeutically, DCA supplementation effectively mitigated trabecular bone loss and improved microarchitectural integrity, while simultaneously regulating white adipose metabolism and hepatic bile acid synthesis. Mechanistically, DCA restores the balance of bone remodeling by promoting osteoblastogenesis over adipogenesis in bone marrow mesenchymal stem cells and inhibiting osteo

Evidence level

Early human evidence such as case series or small samples is exploring possible benefits.

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