METABOLISM OF LPA-I AND LPA-I--A-II IN HUMANS

高密度脂蛋白是异质性的，主要的脂蛋白颗粒包括LPA- I和LPA-I：A-II。目前的数据基于流行病学，细胞培养， 以及转基因动物研究与LPA-I一致 高密度脂蛋白中的抗动脉粥样硬化颗粒。在我们之前的研究中，我们有 确定LPA-I的分解速度快于LPA-I：A-II。 LPA-I：A-II是通过向LPA-I颗粒中添加apoA-II而形成的。 人血浆中存在LPA-I的三个亚类。这三个人 指定为大型、中型和小型的子类具有不同的脂类和 载脂蛋白组成及CETP和LCAT浓度 表明LPA-I粒子的重要不均一性的活度。 女性的血浆浓度高于男性，只有较大的LPA-I 中、小型LPA-I浓度相近的颗粒 粒子。研究了三种LPA-I微粒的代谢。 在正常受试者中。小分子LPA-I的分解代谢是 三个LPA-I粒子中最快的一个，清楚地表明 LPA-I的分解代谢严重依赖于LPA-I的大小 粒子。 深入了解LPA-I和LPA-I的代谢：A-II动力学 研究在50名正常血脂的受试者中进行， 与脂类和载脂蛋白水平的关系已确定。 甘油三酯水平仅与LPA-I呈负相关。载脂蛋白A-I水平 与分解代谢率的相关性最强。载脂蛋白A-II水平 仅与合成速率相关。血浆LPA-I水平为 与apoA-I和apoA-II的分解代谢相关，而LPA-I：A- II水平与apoA-I和apoA-II的合成率相关。 基于多元回归分析，apoA-II的产率为 决定血浆LPA-I的唯一独立动力学参数 级别。进一步的研究正在进行中，以调查其他 调节LPA-I和LPA-I代谢的参数：A-II。 这些研究包括19岁至47岁的受试者。52%的研究 受试者为女性，7人为亚洲人，3人为印度人。

HDL are heterogeneous and the major lipoprotein particles include LpA- I,and LpA-I:A-II. Current data based on epidemiological, cell culture, as well as transgenic animal studies are consistent with LpA-I being the antiatherogenic particle within HDL. In our previous studies we have established that LpA-I is catabolized at a faster rate than LpA-I:A-II. LpA-I:A-II is fromed by the addition of apoA-II to LpA-I particles. Three subclasses of LpA-I are present in human plasma. These three subclasses designated Large, Medium, and Small have different lipid and apolipoprotein composition as well as concentrations of CETP and LCAT activities indicating the important heterogeneity of the LpA-I particles. Women have a higher plasma concentration than men of only the Large LpA-I particle with similar concentration of the Middle and Small LpA-I particles. The metabolism of the three LpA-I particles was investigated in normal control subjects. The catabolism of the Small LpA-I was the fastest of the three LpA-I particles clearly establishing that the catabolism of LpA-I is critically dependent on the size of the LpA-I particle. To gain insight into the metabolism of LpA-I and LpA-I:A-II kinetic studies were performed in fifty normolipidemic subjects and the associations with lipids and apolipoprotein levels determined. Triglyceride levels inversely correlated with only LpA-I. ApoA-I levels were most strongly correlated with the catabolic rate. ApoA-II levels were only correlated with synthesis rate. Plasma LpA-I levels are correlated with the catabolism of both apoA-I and apoA-II while LpA-I:A- II levels were correlated with the synthesis rates of apoA-I and apoA-II. Based on multiple regression analysis the production rate of apoA-II is the only independent kinetic parameter determining the plasma LpA-I levels. Further studies are underway to investigate additional parameters that modulate LpA-I and LpA-I:A-II metabolism. These studies included subjects of age 19 to 47. 52% of the study subjects were women, seven were Asian, and three were Indian.