Institute of Medicine, University of Bergen, Bergen, Norway.
Eur J Nutr. 2013 Jun;52(4):1315-25. doi: 10.1007/s00394-012-0441-2. Epub 2012 Aug 25.
Biological effects of marine oils, fish oil (FO) and krill oil (KO), are mostly attributed to the high content of n-3 polyunsaturated fatty acids (n-3 PUFAs), predominantly eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). The study was aimed to investigate the influence of FO and KO on lipid homeostasis and inflammation in an animal model of persistent low-grade exposure to human tumor necrosis factor α (hTNF-α) and to evaluate whether these effects depend on the structural forms of EPA and DHA [triacylglycerols (TAG) vs. phospholipids].
Male C57BL/6 hTNF-α mice were fed for 6 weeks a high-fat control diet (24.50 % total fats, w/w) or high-fat diets containing either FO or KO at similar doses of n-3 PUFAs (EPA: 5.23 vs. 5.39 wt%, DHA: 2.82 vs. 2.36 wt% of total fatty acids).
We found that KO, containing bioactive n-3 PUFAs in the form of phospholipids, was capable of modulating lipid metabolism by lowering plasma levels of TAG and cholesterol and stimulating the mitochondrial and peroxisomal fatty acid β-oxidation, as well as improving the overall carnitine turnover. Though the administration of FO was not as effective as KO in the lowering of plasma TAG, FO significantly improved the levels of all cholesterol classes in plasma. Except from the increase in the levels of IL-17 in FO-fed mice and a trend to decrease in MCP-1 levels in KO-fed animals, the levels of pro-inflammatory cytokines were not substantially different between treatment groups.
Our findings demonstrate that FO and KO are comparable dietary sources of n-3 PUFAs. However, when quantitatively similar doses of n-3 PUFAs are administered, KO seems to have a greater potential to promote lipid catabolism. The effect of dietary oils on the levels of inflammatory markers in hTNF-α transgenic mice fed a high-fat diet needs further investigations.
海洋油、鱼油（FO）和磷虾油（KO）的生物学效应主要归因于其高度的 n-3 多不饱和脂肪酸（n-3 PUFAs），主要为二十碳五烯酸（EPA）和二十二碳六烯酸（DHA）。本研究旨在研究 FO 和 KO 对持续低水平暴露于人肿瘤坏死因子 α（hTNF-α）的动物模型中脂质稳态和炎症的影响，并评估这些效应是否取决于 EPA 和 DHA 的结构形式[三酰基甘油（TAG）与磷脂]。
雄性 C57BL/6 hTNF-α 小鼠用高脂肪对照饮食（24.50%总脂肪，w/w）或含类似剂量 n-3 PUFAs（EPA：5.23 与 5.39%wt%，DHA：2.82 与 2.36%wt%总脂肪酸）的 FO 或 KO 喂养 6 周。
我们发现，含有生物活性 n-3 PUFAs 形式的磷虾油的 KO，能够通过降低血浆 TAG 和胆固醇水平并刺激线粒体和过氧化物酶体脂肪酸β-氧化，以及改善整体肉碱周转率来调节脂质代谢，尽管 FO 的给药效果不如 KO 降低血浆 TAG 有效，但 FO 显著改善了所有胆固醇类别的血浆水平。除了 FO 喂养的小鼠中 IL-17 水平增加以及 KO 喂养动物中 MCP-1 水平呈下降趋势外，各组之间促炎细胞因子的水平没有明显差异。
我们的发现表明，FO 和 KO 是 n-3 PUFAs 的相当的膳食来源。然而，当给予定量相似剂量的 n-3 PUFAs 时，KO 似乎具有更大的促进脂肪分解的潜力。饮食油对高脂肪饮食喂养的 hTNF-α 转基因小鼠中炎症标志物水平的影响需要进一步研究。
