FISH OILS AND LIPOPROTEIN METABOLISM

吃鱼的人心血管疾病发病率低 这导致了一种假设，即含有鱼油的 ω-3脂肪酸（ω 3FA）可以是保护剂。 临床 研究表明，高摄入量的鱼油会导致 胆固醇，特别是甘油三酯水平下降， 和高血压患者。 尽管在这些研究中， 密度脂蛋白（LDL）胆固醇水平降低，最近 使用更实际的鱼油摄入量的研究（少于20 gm/天）发现LDL胆固醇显著升高 尤其是高甘油三酯血症（HTG）患者。 因此，鱼油在这一人群中的作用可能有限。 我们建议研究极低密度脂蛋白（VLDL）和LDL 在32名服用鱼油的HTG患者中， 植物油对照。 他们将收到12粒1克的 油每天2，随机分配，6周的时间。 在8 HTG家族性混合型高脂血症（FCHL）患者和8例 与家族性高脂血症（FHTG），动力学2 VLDL亚组分将在两个阶段中的每个阶段进行研究。 治疗阶段。 在8个FCHL和8个FHTG的不同组中， 患者，将进行LDL动力学研究。 此外， VLDL和LDL的化学成分将通过以下方法测量： 超离心和柱层析相结合， HTG患者组和8名正常受试者组。 我们 应该能够确定LDL的增加是否 服用鱼油补充剂的HTG患者的胆固醇是 结果1）大和/或小VLDL转化为 LDL，2）LDL的直接肝分泌，3）LDL的清除减少， 血浆中的LDL，因为竞争增加， 小VLDL的清除机制，或4）减少清除 由于w3 FA对受体或非受体的直接作用， 受体介导的途径。 这些研究应该揭示 w3 FA补充剂改变脂蛋白的机制 HTG患者的代谢。

The low incidence of cardiovascular diseases among fish-eating populations has led to the hypothesis that fish oils containing omega-3 fatty acids (w3 FA) may be protective agents. Clinical studies have shown that high intakes of fish oils cause total cholesterol and, particularly, triglyceride levels to fall in normals and hyperlipidemic patients. Although in these studies low density lipoprotein (LDL) cholesterol levels were reduced, recent studies utilizing more practical intakes of fish oil (less than 20 gm/day) have found significant elevations in LDL cholesterol levels, especially in patients with hypertriglyceridemia (HTG). Thus, the usefulness of fish oil may be limited in this population. We propose to study very low density lipoprotein (VLDL) and LDL apolipoprotein B metabolism in 32 HTG patients given fish oil vs. a vegetable oil control. They will receive 12, 1-gm capsules of the oils per day for 2, randomly assigned, 6-week periods. In 8 HTG patients with familial combined hyperlipidemia (FCHL) and 8 with familial hypertriglyceridemia (FHTG), the kinetics of 2 VLDL subfractions will be studied during each of the two treatment phases. In a different group of 8 FCHL and 8 FHTG patients, LDL kinetic studies will be done. Also, changes in the chemical composition of VLDL and LDL will be measured by combined ultracentrifugation and column chromatography in both groups of HTG patients and in a group of 8 normal subjects. We should be able to determine whether the increase in LDL cholesterol in HTG patients given fish oil supplements is the result of 1) increased conversion of large and/or small VLDL to LDL, 2) direct hepatic secretion of LDL, 3) decreased removal of LDL from the plasma because of increased competition from small VLDL for removal mechanisms, or 4) decreased removal of LDL because of a direct effect of w3 FA on receptor or non- receptor mediated pathways. These studies should reveal the mechanisms by which w3 FA supplements alter lipoprotein metabolism in HTG patients.