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Neonatal low-bacterial-load during lactation impairs peak bone mass via a gut-liver-bone axis
Yingchu Zhao1, Wenwen Luo2, Tingyu Chen2
1Laboratory of Tissue Regeneration and Immunology and Department of Periodontics, Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction, Capital Medical University School of Stomatology, Beijing, China.
Biochemical and Biophysical Research Communications
|June 3, 2026
Summary
Early-life low gut bacteria disrupt bone development. This study reveals how reduced gut microbiota in infancy impairs peak bone mass in adulthood by altering gut-liver-bone axis signaling.
Area of Science:
- Microbiology
- Bone Biology
- Metabolism
Background:
- Peak bone mass (PBM) is crucial for preventing adult osteoporosis and fractures.
- The gut microbiota influences bone health, but its early-life impact on PBM is not well understood.
- Lactation is a critical window for gut microbiota development.
Purpose of the Study:
- To investigate the long-term effects of low early-life gut bacterial load on PBM in adulthood.
- To elucidate the mechanisms linking early gut dysbiosis to impaired bone acquisition.
Main Methods:
- Established a neonatal antibiotic exposure (NeoATB) mouse model to simulate low lactation-period bacterial load.
- Analyzed gut microbiota composition using longitudinal 16S rRNA sequencing.
- Performed fecal metabolomic profiling, hepatic lipid analysis, and functional assays on osteoclast differentiation.
Main Results:
- NeoATB mice showed significantly reduced femoral PBM and increased osteoclast activity at 24 weeks.
- Low bacterial load led to persistent gut microbiota alterations, hepatic lipid accumulation, and increased circulating palmitic acid.
- Palmitic acid directly promoted osteoclast differentiation from monocytes.
Conclusions:
- Neonatal low bacterial load disrupts the gut microbiota and reprograms hepatic lipid metabolism.
- This process increases serum fatty acids, driving excessive osteoclast differentiation and reducing PBM.
- The gut-liver-bone axis is a key pathway through which early-life gut dysbiosis impairs adult bone mass.
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