Hyodeoxycholic acid and bone marrow stromal cells in postmenopausal osteoporosis: an abstract
In this abstract, serum hyodeoxycholic acid was most reduced in postmenopausal osteoporosis patients and correlated negatively with bone marrow stromal cell senescence and adipogenesis; in mice, oral hyodeoxycholic acid reversed bone architecture deterioration. [1]
Automatic summary · not editorially reviewed
The key findings
Serum hyodeoxycholic acid showed the largest reduction among differential bile acids in postmenopausal osteoporosis patients and correlated negatively with bone marrow stromal cell senescence and adipogenesis. [1]
Exogenous hyodeoxycholic acid dose-dependently inhibited senescence and corrected aberrant adipogenesis in patient-derived bone marrow stromal cells. [1]
In ovariectomized mice, oral hyodeoxycholic acid replenished systemic levels, reversed bone architecture deterioration and activated TGR5-ESR1 signaling in intestinal and bone tissues. [1]
The source at a glance
- Study type / format
- Abstract of a laboratory and animal study with patient samples
- Population / context
- Postmenopausal osteoporosis patients, healthy donors, patient-derived bone marrow stromal cells and ovariectomized mice.
- Summary based on
- Study abstract
- Original publication
- October 10, 2026
Bile acid profiles in osteoporosis patients versus donors
The abstract describes serum bile acid profiling in postmenopausal osteoporosis patients and healthy donors. Among the differential bile acids, hyodeoxycholic acid (HDCA) showed the largest reduction in patients. Its serum levels correlated negatively with bone marrow stromal cell (BMSC) senescence and adipogenesis. The abstract frames postmenopausal osteoporosis as driven by BMSC senescence and aberrant adipogenesis, with 17β-estradiol deficiency as a primary trigger, and states that the metabolic link between systemic estradiol loss and BMSC dysfunction was previously undefined.
Supporting source [1]
HDCA effects on patient-derived BMSCs and proposed pathway
Patient-derived BMSCs treated with exogenous HDCA showed dose-dependent inhibition of senescence and correction of aberrant adipogenesis. Mechanistically, the abstract reports that HDCA bound the membrane receptor TGR5 with higher affinity than the nuclear farnesoid X receptor (FXR), activating a cAMP-PKA cascade that raises ESR1 (estrogen receptor 1) expression and triggers PINK1/Parkin-mediated mitophagy, a mitochondrial quality-control process. These mechanism findings came from molecular docking, RNA sequencing and pharmacological or genetic interventions, including an H2O2-induced senescence model, TGR5/ESR1 knockdown and PKA inhibition.
Supporting source [1]
Oral HDCA in ovariectomized mice and abstract limits
In ovariectomized (OVX) mice, oral HDCA administration replenished systemic HDCA levels, reversed bone architecture deterioration and activated TGR5-ESR1 signaling in both intestinal and bone tissues. The abstract concludes that HDCA supplementation alleviates BMSC senescence and aberrant adipogenesis through this axis and provides a basis for non-hormonal strategies for postmenopausal osteoporosis. These are preclinical and cell-model findings; the abstract reports no human treatment trial, and the mouse results do not establish benefit in people. Only the abstract was reviewed; the full text was not reviewed.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. Findings include cell models and ovariectomized mice, with no human treatment trial reported. Associations in patients are not causal, and mouse results do not establish benefit in people.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Zeng C, Yu W, Kang Y, Liu W, Chen Z, Xiao Z, Liu Z, Zhang W, Li Q, Zeng Y, Li Z, Pan B, Xie Z, Zhang Z. · europepmc.org · October 10, 2026