n-3 fatty acids reduce arterial LDL-cholesterol delivery and arterial lipoprotein lipase levels and lipase distribution.
n-3 fatty acids reduce arterial LDL-cholesterol delivery and arterial lipoprotein lipase levels and lipase distribution.
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DOI：
10.1161/atvbaha.108.182287
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发表时间：
2009-04
期刊：
影响因子：
--
通讯作者：
Deckelbaum RJ
中科院分区：
文献类型：
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作者：
Chang CL;Seo T;Matsuzaki M;Worgall TS;Deckelbaum RJ
我们以前报道过，富含饱和脂肪(SAT)的饮食增加了动脉胆固醇酯(CE)的沉积，特别是通过低密度脂蛋白选择性摄取(SU)，这与动脉脂蛋白脂酶(LPL)的增加有关。我们现在质疑富含n-3脂肪酸的饮食如何影响动脉胆固醇输送和动脉LPL水平。C57BL/6小鼠饲喂高脂饲料或高脂饲料12周，然后注射双标记或荧光标记的人低密度脂蛋白，分别示踪低密度脂蛋白-CE和低密度脂蛋白-载脂蛋白B摄取。SAT和n-3饮食类似地增加了血浆胆固醇水平；n-3饮食降低了血浆甘油三酯浓度。Sat可增加动脉低密度脂蛋白-SU，显著增加CE对主动脉中层的浸润率。相反，n-3显著减少了总的低密度脂蛋白摄取和CE沉积，并取消了低密度脂蛋白仅定位于主动脉内膜的SU。不同饮食之间CE沉积的不同模式与动脉LPL-SAT饮食导致整个主动脉LPL水平升高的分布一致；n-3饮食降低LPL水平并限制LPL在主动脉内膜的表达。在改变动脉壁LPL的表达和分布的同时，富含N-3的饮食减少了动脉总低密度脂蛋白的供应，并消除了低密度脂蛋白-SU。
We previously reported that saturated fat (SAT) enriched diets increase arterial cholesteryl ester (CE) deposition, especially from LDL-selective uptake (SU), and this was associated with increased arterial lipoprotein lipase (LpL). We now questioned how n-3 fatty acid rich diets influence arterial cholesterol delivery and arterial LpL levels. C57BL/6 mice were fed chow or eucaloric high fat diets enriched in SAT or fish oil (n-3) for 12 weeks, and then injected with double radiolabeled or fluorescent-labeled human LDL to separately trace LDL-CE and LDL-apoB uptake. SAT and n-3 diets increased plasma cholesterol levels similarly; n-3 diets lowered plasma triglyceride concentrations. SAT increased arterial LDL-SU with significantly higher CE infiltration into aortic media. In contrast, n-3 markedly reduced total LDL uptake and CE deposition and abolished SU with LDL localized only in aortic intima. Disparate patterns of CE deposition between diets were consistent with distribution of arterial LpL - SAT diets induced higher LpL levels throughout the aorta; n-3 diets decreased LpL levels and limited LpL expression to the aortic intima. n-3 rich diets decrease arterial total LDL delivery and abrogate LDL-SU in parallel with changing arterial wall LpL expression and distribution.