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反式-10,顺式-12 共轭亚油酸通过过氧化物酶体增殖物激活受体-γ 依赖性机制抑制脂肪生成,并通过直接增强骨髓间充质干细胞向成骨细胞的分化来促进骨形成。

trans-10,cis-12 conjugated linoleic acid promotes bone formation by inhibiting adipogenesis by peroxisome proliferator activated receptor-γ-dependent mechanisms and by directly enhancing osteoblastogenesis from bone marrow mesenchymal stem cells.

机构信息

Department of Food Science, University of Massachusetts, Amherst, MA 01003, USA.

出版信息

J Nutr Biochem. 2013 Apr;24(4):672-9. doi: 10.1016/j.jnutbio.2012.03.017. Epub 2012 Jul 23.

Abstract

The bone undergoes continuous remodeling of osteoblastic bone formation and osteoclastic bone resorption to maintain proper bone mass. It is also reported that bone marrow adiposity has a reciprocal role in osteoblasts due to their same origin from mesenchymal stem cells. In addition, one of the key mediators of adipogenesis, peroxisome-proliferator activated receptor-γ (PPARγ), plays a significant role in osteoblastogenesis in bone marrow mesenchymal stem cells. One dietary component that is known to have significant impact on adiposity and bone mass is conjugated linoleic acid (CLA). However, the link between controlling adiposity to improving bone mass by CLA has not been studied intensively. Thus, the purpose of this study is to determine the role of CLA on bone marrow adiposity and bone formation using murine mesenchymal stem cells. The results confirmed that the trans-10,cis-12 CLA, but not the cis-9,trans-11 CLA isomer, significantly inhibited adipogenesis and promoted osteoblastogenesis from mesenchymal stem cells. The inhibition of adipogenesis by the trans-10,cis-12 CLA was mediated by PPARγ; however, the trans-10,cis-12 CLA had a direct effect on osteoblastogenesis which was independent to PPARγ in this model. The trans-10,cis-12 CLA also had significant effects on osteoclastogenesis inhibitory factor, which suggests potential influence of CLA on osteoclastogenesis. Overall, the results suggest that the trans-10,cis-12, but not the cis-9,trans-11 CLA isomer, has a positive impact on bone health by both PPARγ mediated and independent mechanisms in mesenchymal stem cells.

摘要

骨骼通过成骨细胞的骨形成和破骨细胞的骨吸收进行持续的重塑,以维持适当的骨量。据报道,由于骨髓间充质干细胞起源相同,骨髓脂肪含量对成骨细胞具有相反的作用。此外,脂肪生成的关键介质之一过氧化物酶体增殖物激活受体-γ(PPARγ)在骨髓间充质干细胞中的成骨细胞生成中发挥重要作用。已知有一种饮食成分对脂肪含量和骨量有显著影响,那就是共轭亚油酸(CLA)。然而,CLA 通过控制脂肪含量来改善骨量的作用机制尚未得到深入研究。因此,本研究的目的是使用鼠骨髓间充质干细胞来确定 CLA 对骨髓脂肪含量和骨形成的作用。结果证实,反式-10,顺式-12CLA,但不是顺式-9,反式-11CLA 异构体,显著抑制脂肪生成并促进骨髓间充质干细胞的成骨细胞生成。反式-10,顺式-12CLA 对脂肪生成的抑制作用是通过 PPARγ介导的;然而,在该模型中,反式-10,顺式-12CLA 对成骨细胞生成具有直接作用,与 PPARγ无关。反式-10,顺式-12CLA 对破骨细胞生成抑制因子也有显著影响,这表明 CLA 对破骨细胞生成可能有潜在影响。总的来说,这些结果表明,反式-10,顺式-12CLA(而不是顺式-9,反式-11CLA 异构体)通过 PPARγ 介导和独立的机制对骨髓间充质干细胞的骨健康产生积极影响。

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