FISH OILS AND LIPOPROTEIN METABOLISM

食鱼人群心血管疾病发病率低 种群数量导致了这样的假设，即鱼油中含有 Omega-3脂肪酸(W3FA)可能是保护剂。临床 研究表明，大量摄入鱼油会导致 胆固醇，特别是甘油三酯水平将在正常情况下下降 和高脂血症患者。尽管在这些研究中 密度脂蛋白(LDL)胆固醇水平最近有所下降 研究利用更实际的鱼油摄入量(不到20 GM/day)发现低密度脂蛋白胆固醇显著升高 尤其是在高甘油三酯血症(HTG)患者。 因此，鱼油在这一群体中的用处可能有限。 我们建议研究极低密度脂蛋白(VLDL)和低密度脂蛋白 32例服用鱼油的HTG患者的载脂蛋白B代谢。 植物油控制剂。他们将收到12，1-gm胶囊 每天服用2次，随机分配，为期6周。在8年内 家族性混合性高脂血症(FCHL)合并HTG患者8例 家族性高甘油三酯血症时，2 极低密度脂蛋白亚组分将在这两个过程中分别进行研究 治疗阶段。在8个FCHL和8个FHTG不同组中 患者，将进行低密度脂蛋白动力学研究。此外，还将更改 极低密度脂蛋白和低密度脂蛋白的化学成分将通过 超速离心法与柱层析联用技术在两者中的应用 HTG患者组和正常对照组各8例。我们 应该能够确定低密度脂蛋白的增加 服用鱼油补充剂的HTG患者的胆固醇是 结果1)较大和/或较小极低密度脂蛋白转换为 2)肝脏直接分泌低密度脂蛋白，3)减少清除 血浆中的低密度脂蛋白，因为来自 较小的极低密度脂蛋白用于去除机制，或4)减少去除 低密度脂蛋白因w3FA对受体或非受体的直接作用 受体介导的通路。这些研究应该会揭示 补充w3脂肪酸改变脂蛋白的机制 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.