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采用胆固醇脂转运蛋白（CETP）介导极低密度脂蛋白（VLDL）中甘油三酯（TG）与低密度脂蛋白（LDL）中胆固醇（CH）交换：再行脂蛋白脂酶（LPL）水解LDL中TG，对LDL进行修饰，引起LDL颗粒组成和大小的变化，探讨体内小而致密的LDL形成的可能途径，及易于致动脉粥样硬化（As）作用的机制。结果示CETP介导的脂质转运使LDL中TG含量增加，CH降低，颗粒直径轻微变大；再经LPL水解的共同作用，LDL中TG含量降低，颗粒变小。同时LDL中载脂蛋白B（apoB）免疫反应性也发生相应的变化，LDL中TG含量同apoB免疫反应性高度负相关。认为大而轻的A型LDL经修饰作用可转变为小而致密的B型LDL，富含TG的LDL不易于通过apoB受体途径清除，史易于氧化。
Cholesterol (CH) exchange between triglyceride (TG) and low density lipoprotein (LDL) in very low density lipoprotein (VLDL) is mediated by cholesterol lipid transporter (CETP): Lipoprotein lipase (LPL) LDL in TG, the modification of LDL, LDL particles caused by changes in the composition and size of the body to explore the possible ways of small and dense formation of LDL, and easy to cause atherosclerosis (As) mechanism. The results showed that CETP-mediated lipid transport increased LDL TG content, CH decreased slightly larger particle diameter; and LPL hydrolysis by the combined effect of LDL TG content decreased, the particles become smaller. At the same time, the apoB immunoreactivity in LDL also changed accordingly. The content of TG in LDL was highly negatively correlated with apoB immunoreactivity. It is believed that the large and light A-type LDL can be modified to small and compact B-type LDL. TG-rich LDL is not easily cleared by the apoB receptor pathway, and its history is easy to be oxidized.