众所周知，饮酒会导致骨质流失，骨密度与骨髓脂肪细胞(BMA)呈反比关系。然而，关于酒精和骨质流失的联系机制鲜为人知，现有研究也缺乏有关酒精引起的骨质流失中BMA的数据。在这项研究中，使用野生型(WT)和肿瘤坏死因子-α敲除(TNF-α KO)小鼠来检查酒精对骨代谢的影响。通过给WT和TNF-α KO小鼠喂酒展示了酒精对骨代谢的影响。比较了从WT和TNF-α KO小鼠中获得的初级骨髓基质细胞(BMSCs)在酒精干预下的成骨和成脂能力。使用组织染色、细胞染色、微CT和定量RT-PCR来探讨潜在机制。酒精诱导WT小鼠的骨小梁骨量下降、BMA增加并促进了BMA中Adipoq、Fabp4、visfatin、Pparg、TNF-α、IL-1β和IL-6的mRNA表达，但在TNF-α KO小鼠中没有这种情况。此外，酒精促进BMSC成脂并抑制BMSC成骨，而TNF-α敲除可以抑制这种状况。本研究表明，酒精可能通过破坏骨髓成骨和成脂的平衡来减少骨量，而TNF-α在这个过程中起着重要的作用。©2023年作者。 Medical Council on Alcohol和Oxford University Press保留所有权利。关于权限，请发送电子邮件至：journals.permissions@oup.com。

It is well known that alcohol can cause bone loss and that bone mineral density has an inverse relationship with bone marrow adipocyte (BMA). However, little is known about the mechanisms that link alcohol and bone loss, and existing studies lack data on BMA in alcohol-induced bone loss. Here, wild-type (WT) and tumor necrosis factor-alpha knockout (TNF-α KO) mice were used to examine the effects of alcohol on bone metabolism.The effects of alcohol on bone metabolism were demonstrated in vivo by feeding WT and TNF-α KO mice with alcohol. The osteogenesis and adipogenesis of primary bone marrow stromal cells (BMSCs) derived from WT and TNF-α KO mice under alcohol intervention were compared in vitro. Tissue staining, cell staining, micro-CT, and quantitative RT-PCR were used to explore the potential mechanism.Alcohol induced trabecular bone loss, increased BMA, and promoted the mRNA expression of Adipoq, Fabp4, visfatin， Pparg, TNF-α, IL-1β, and IL-6 in BMA in WT mice, but not in TNF-α KO mice. In addition, alcohol promoted BMSC adipogenesis and inhibited BMSC osteogenesis, while TNF-α knockout could restrain this situation.Our study demonstrated that alcohol may reduce bone mass by disrupting the balance of osteogenesis and adipogenesis in bone marrow, and TNF-α plays an important role in this process.© The Author(s) 2023. Medical Council on Alcohol and Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.