Shirakura Yoshiyuki, Takayanagi Katsuhiko, Mukai Katsuyuki, Tanabe Hiroki, Inoue Makoto
Research and Development Center, Unitika Ltd, Uji, Kyoto, Japan.
J Nutr Sci Vitaminol (Tokyo). 2011;57(6):426-31. doi: 10.3177/jnsv.57.426.
We recently reported that the oral intake of β-cryptoxanthin exerted anti-obesity effects by lowering visceral fat levels. In the present study, we characterized the molecular mechanisms underlying the lipid-lowering effects of β-cryptoxanthin on 3T3-L1 cells. Consistent with our previous findings, β-cryptoxanthin rapidly reduced the level of intracellular lipids in 3T3-L1 cells as assessed by Oil red O staining. Using an in vitro nuclear receptor binding assay, we demonstrated the ability of β-cryptoxanthin to bind to and activate members of the retinoic acid receptor (RAR) family. Accordingly, treatment of cells with LE540, an RAR antagonist, abolished the β-cryptoxanthin-dependent suppression of 3T3-L1 adipogenesis, suggesting that β-cryptoxanthin mediates its effects on 3T3-L1 cells via RAR activation. In addition, real-time RT-PCR analysis revealed that β-cryptoxanthin down-regulates mRNA expression of PPARγ, a key regulator of adipocyte differentiation, and that this inhibition was blocked by LE540 treatment. Taken together, these data indicate that RAR activation contributes to the molecular mechanism by which β-cryptoxanthin prevents obesity.
我们最近报道，口服β-隐黄质通过降低内脏脂肪水平发挥抗肥胖作用。在本研究中，我们阐述了β-隐黄质对3T3-L1细胞降脂作用的分子机制。与我们之前的研究结果一致，通过油红O染色评估，β-隐黄质可迅速降低3T3-L1细胞内脂质水平。使用体外核受体结合试验，我们证明了β-隐黄质与视黄酸受体（RAR）家族成员结合并激活它们的能力。因此，用RAR拮抗剂LE540处理细胞，消除了β-隐黄质对3T3-L1脂肪生成的依赖性抑制，表明β-隐黄质通过RAR激活介导其对3T3-L1细胞的作用。此外，实时RT-PCR分析显示，β-隐黄质下调脂肪细胞分化关键调节因子PPARγ的mRNA表达，并且这种抑制作用被LE540处理所阻断。综上所述，这些数据表明RAR激活是β-隐黄质预防肥胖的分子机制之一。
