首页> 外文期刊>The Journal of Nutrition: Official Organ of the American Institute of Nutrition >(n-3) Fatty Acid Supplementation in Moderately Hypertriglyceridemic Adults Changes Postprandial Lipid and Apolipoprotein B Responses to a Standardized Test Meal
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(n-3) Fatty Acid Supplementation in Moderately Hypertriglyceridemic Adults Changes Postprandial Lipid and Apolipoprotein B Responses to a Standardized Test Meal

机译:(n-3)中度高甘油三酯血症成年人中的脂肪酸补充改变了餐后脂质和载脂蛋白B对标准测试餐的反应

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The effects of (n-3) fatty acids on the postprandial state were investigated by monitoring the alimentary responses to identical test meals fed to adults [n = 11; fasting triacylglycerol (TG) 2.55 ± 0.24 mmol/L; mean ± sem] after a self-selected diet baseline period (BLP) and then after a 6-wk (n-3) fatty acid period (FOP) [~5.2 g (n-3) fatty acids] and a 6-wk control oil period (COP) administered in random order. Samples were drawn immediately prior to the test meal (time 0) and then hourly from 2 to 6 h postmeal. Postprandial plasma triacylglycerol (TG) and TG-rich lipoprotein (TRL) TG apo B48, and B100 absolute concentrations were significantly lower after FOP than after COP or BLP, while plasma cholesterol was unchanged. Normalizing the results as increments over time 0 eliminated the diet effect on all but plasma TG. Time remained a significant effect for plasma TG, TRL TG, and TRL TC. Finally, only absolute TRL B48 and absolute and incremental plasma TG concentrations displayed significant time-diet interactions. These results suggest that postprandial TRL apo B reductions are likely caused by (n-3) fatty acid suppression of both hepatic and intestinal apoB secretion/synthesis. Altered TRL metabolism, i.e. changes in postprandial TG, cholesterol, apo B48, and increase in LDL particle size, may represent an additional mechanism for the reduced heart disease risk associated with fish [(n-3) fatty acid] consumption.
机译:(n-3)脂肪酸对餐后状态的影响是通过监测对成年人喂食的相同测试膳食的营养反应进行调查的[n = 11;空腹甘油三酯(TG)2.55±0.24 mmol / L;均值±sem]在自选饮食基线期(BLP)之后,然后在6周(n-3)脂肪酸期(FOP)[〜5.2 g(n-3)脂肪酸]和6周控制油期(COP)随机给药。在就餐前(时间0)立即取样,然后在餐后2至6小时每小时取样。餐后血浆三酰基甘油(TG)和富含TG的脂蛋白(TRL)TG apo B48和B100的绝对浓度均显着低于COP或BLP后,而血浆胆固醇未发生变化。将结果标准化为随时间0的增加,可以消除除血浆TG以外的所有食物的饮食影响。时间对于血浆TG,TRL TG和TRL TC仍然具有重大影响。最后,只有绝对TRL B48以及绝对和增量血浆TG浓度显示出显着的时间-饮食相互作用。这些结果表明,餐后TRL载脂蛋白B的减少很可能是由(n-3)脂肪酸抑制肝和肠道载脂蛋白B分泌/合成引起的。 TRL代谢改变,即餐后TG,胆固醇,载脂蛋白B48的变化和LDL粒径的增加,可能代表了降低与鱼类[(n-3)脂肪酸]食用相关的心脏病风险的另一种机制。

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