Alcohol consumption exacerbates high-fat diet-mediated disruptions in myelopoiesis and osteoclastogenesis in mouse models of metabolic dysfunction-associated liver diseases
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By
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March 20, 2026
Objective:
To characterize the bone marrow hematopoietic compartment and its link to osteoclastogenesis in mouse models of MASLD and MetALD, focusing on specific hematopoietic alterations.
Key Findings:
- HFD depletes hematopoietic stem cells (HSC) and early multipotent progenitors.
- HFD+EtOH preserves HSC and skews hematopoiesis toward myeloid-committed progenitors.
- Increased osteoclast precursors (CD115+RANK+) and enhanced osteoclastogenesis in HFD+EtOH compared to HFD alone.
- Elevated osteoclast activity and changes in bone morphology in HFD+EtOH-fed mice.
Interpretation:
Alcohol amplifies the effects of a high-fat diet on hematopoiesis and osteoclast formation, suggesting a need for attention to hematopoietic health in MASLD and MetALD patients, particularly in managing immune and skeletal complications.
Limitations:
- Study conducted in mouse models may not fully translate to human conditions.
- Limited understanding of the molecular mechanisms underlying the observed changes.
- Potential variability in mouse models compared to human conditions.
Conclusion:
Findings indicate that both HFD and HFD+EtOH induce diet-specific hematopoietic alterations, with alcohol exacerbating these effects, highlighting the importance of addressing immune and skeletal complications in metabolic liver diseases.
