Shibata Akira, Kobayashi Teiko, Asai Akira, Eitsuka Takahiro, Oikawa Shinichi, Miyazawa Teruo, Nakagawa Kiyotaka
Food and Biodynamic Chemistry Laboratory, Graduate School of Agricultural Science, Tohoku University, Sendai 981-8555, Japan.
Food and Health Science Research Unit, Graduate School of Agricultural Science, Tohoku University, Sendai 981-8555, Japan; Department of Endocrinology, Diabetes and Metabolism, Graduate School of Medicine, Nippon Medical School, Tokyo 113-0023, Japan.
J Nutr Biochem. 2017 Oct;48:44-50. doi: 10.1016/j.jnutbio.2017.06.009. Epub 2017 Jun 24.
Previous studies have demonstrated that tocotrienol (T3) has antiatherogenic effects. However, the T3 preparations used in those studies contained considerable amounts of tocopherol (Toc), which might affect the biological activity of T3. There is little information on the effect of highly purified T3 on atherosclerosis formation. This study investigated the effect of high-purity T3 on atherosclerotic lesion formation and the underlying mechanisms. Male apolipoprotein E knockout (apoE-KO) mice were fed a cholesterol-containing diet either alone or supplemented with T3 concentrate (Toc-free T3) or with α-Toc for 12 weeks. ApoE-KO mice fed the 0.2% T3-supplemented diet showed reduced atherosclerotic lesion formation in the aortic root. The 0.2% T3 diet induced Slc27a1 and Ldlr gene expression levels in the liver, whereas the α-Toc-supplemented diet did not affect those expression levels. T3 was predominantly deposited in fat tissue in the T3 diet-fed mice, whereas α-Toc was preferentially accumulated in liver in the α-Toc diet-fed mice. Considered together, these data demonstrate that dietary T3 exerts anti-atherosclerotic effect in apoE-KO mice. The characteristic tissue distribution and biological effects of T3, that are substantially different from those of Toc, may contribute to the antiatherogenic properties of T3.
先前的研究表明,生育三烯酚(T3)具有抗动脉粥样硬化作用。然而,那些研究中使用的T3制剂含有大量的生育酚(Toc),这可能会影响T3的生物活性。关于高纯度T3对动脉粥样硬化形成的影响,相关信息较少。本研究调查了高纯度T3对动脉粥样硬化病变形成的影响及其潜在机制。雄性载脂蛋白E基因敲除(apoE-KO)小鼠单独喂食含胆固醇的饮食,或补充T3浓缩物(不含Toc的T3)或α-Toc,持续12周。喂食补充0.2% T3饮食的apoE-KO小鼠主动脉根部的动脉粥样硬化病变形成减少。0.2% T3饮食诱导肝脏中Slc27a1和Ldlr基因表达水平升高,而补充α-Toc的饮食对这些表达水平没有影响。在喂食T3饮食的小鼠中,T3主要沉积在脂肪组织中,而在喂食α-Toc饮食的小鼠中,α-Toc优先在肝脏中积累。综合来看,这些数据表明,饮食中的T3对apoE-KO小鼠具有抗动脉粥样硬化作用。T3独特的组织分布和生物学效应与Toc有很大不同,这可能是T3具有抗动脉粥样硬化特性的原因。