Hashimoto Toru, Shimizu Naoto, Kimura Toshinori, Takahashi Yoko, Ide Takashi
Division of Food Functionality, National Food Reserach Institute, 2-1-12 Kannondai, Tsukuba 305-8642, Japan.
J Nutr. 2006 Apr;136(4):882-6. doi: 10.1093/jn/136.4.882.
The effects of dietary phytol and the type of dietary fat on hepatic fatty acid oxidation were examined in male ICR mice. Mice were fed diets containing 0 or 5 g/kg phytol and 100 g/kg palm, safflower, or fish oil for 21 d. Among the groups fed phytol-free diets, the activities and mRNA abundance of various enzymes involved in fatty acid oxidation were greater in mice fed fish oil than in those fed palm or safflower oil. Dietary phytol profoundly increased the activities and mRNA abundance of hepatic fatty acid oxidation enzymes in mice fed palm oil. However, safflower and fish oils, especially the latter, greatly attenuated the phytol-dependent increase in hepatic fatty acid oxidation. The hepatic concentration of phytanic acid, a metabolite of phytol that is the ligand and activator of retinoid X receptors and peroxisome proliferator-activated receptors, was higher in mice fed fish oil than safflower or palm oil, and in those administered safflower oil than palm oil. The hepatic mRNA abundance of sterol carrier protein-2, a lipid-binding protein involved in phytol metabolism, was inversely correlated with the hepatic concentration of phytanic acid. We demonstrated that polyunsaturated fats attenuate the enhancing effect of dietary phytol on hepatic fatty acid oxidation. Dietary fat-dependent changes in the hepatic phytanic acid concentration cannot account for this phenomenon.
在雄性ICR小鼠中研究了膳食叶绿醇和膳食脂肪类型对肝脏脂肪酸氧化的影响。给小鼠喂食含0或5 g/kg叶绿醇以及100 g/kg棕榈油、红花油或鱼油的饲料，持续21天。在喂食不含叶绿醇饲料的组中，脂肪酸氧化相关的各种酶的活性和mRNA丰度在喂食鱼油的小鼠中高于喂食棕榈油或红花油的小鼠。膳食叶绿醇显著增加了喂食棕榈油小鼠肝脏脂肪酸氧化酶的活性和mRNA丰度。然而，红花油和鱼油，尤其是后者，极大地减弱了叶绿醇依赖性的肝脏脂肪酸氧化增加。植烷酸是叶绿醇的一种代谢产物，是视黄醇X受体和过氧化物酶体增殖物激活受体的配体和激活剂，其在肝脏中的浓度在喂食鱼油的小鼠中高于喂食红花油或棕榈油的小鼠，在喂食红花油的小鼠中高于喂食棕榈油的小鼠。固醇载体蛋白2是一种参与叶绿醇代谢的脂质结合蛋白，其肝脏mRNA丰度与肝脏植烷酸浓度呈负相关。我们证明了多不饱和脂肪减弱了膳食叶绿醇对肝脏脂肪酸氧化的增强作用。肝脏植烷酸浓度的膳食脂肪依赖性变化不能解释这一现象。
