Apolipoprotein-Binding of Artificial Lipid Particles Assocated with Fat Infusion

人工脂颗粒的血管内代谢与乳糜粒非常相似。乳糜粒结合多种载脂蛋白，调节乳糜粒的血管内代谢，而人工脂颗粒不含任何载脂蛋白。对人工脂颗粒的载脂蛋白结合机理进行了研究。研究结果总结如下：1.人工脂颗粒进入血液后，立即从高密度脂蛋白中获得载脂蛋白C-II、C-III和E。人工脂颗粒水解后，载脂蛋白C-II和C-III回到高密度脂蛋白，而载脂蛋白E残留在脂颗粒上。人工脂颗粒与载脂蛋白的结合只是由于载脂蛋白与脂粒表面的亲水性自由基的亲和力所致。根据脂肪输注速度的不同，高密度脂蛋白将载脂蛋白C捐献给人造脂颗粒的能力是有限的。没有结合apoC的脂肪颗粒可能会被网状内皮系统摄取，因为这种类型的脂肪颗粒在人类中通常不存在。因此，在临床环境中，不以0.1gTg/kg/h的速度注入脂肪乳剂是更合适的。

The intravascular metabolism of artificial lipid particles is quite similar to that of chylomicrons. Chylomicrons bind various kinds of apolipoprotein that regulate intravascular metabolism of chylomicrons, while artificial lipid particles do not contain any apolipoproteins. Apolipoprotein-binding mechanisms of artificial lipid particles were inverstigated. The research results are summarized as follows ;1. Artificial lipid particles acquire apolipoproteins C-II, C-III and E from high-density lipoprotein (HDL), immediately after their entry into bloodstream.2. Apolipoproteins C-II and C-III return to HDL after the hydrolysis of artificial lipid particles, while apolipoprotein E remains on the remnants of lipid particles.3. Artificial lipid particles bind apolipoproteins simply as the result of affinity of apolipoproteins for hydrophilic radicals on the surface of lipid particles.4. Depending on the rate of fat infusion, there is a limit to the capacity of HDL for donating apoC to artificial lipid particles. Fat particles that do not bind apoC may undergo the uptake by the reticulo-endothelial system, because this type of fat particle does not normally exist in humans. Accordingly, it is more appropriate not to infuse an emulsion of fat at a rate >0.1g TG/kg/h in a clinical setting.