论文部分内容阅读
脂蛋白脂酶(LL)和肝脏甘油三酯脂酶(HTL)都与乳糜微粒(CM)和极低密度脂蛋白(VLDL)的甘油三酯的水解有关。LL的活性与载脂蛋白CⅡ(ApoCⅡ)有必然联系。本文将从生化和临床角度对LL缺乏(家族性高脂蛋白血症Ⅰ型),HTL缺乏和ApoCⅡ缺乏进行探讨。乳糜微粒(CM)和极低密度脂蛋白(VLDL)中甘油三酯的水解至少有两种酶催化,即脂蛋白脂酶(LL)和肝脏甘油三酯脂酶(HTL)。它们都是糖蛋白,均存在于毛细血管的内皮细胞中。LL和HTL的主要区别是LL的完全活化依赖于ApoCⅡ。ApoCⅡ对LL的活性是一个复合因子,而HTL的活性
Both lipoprotein lipase (LL) and hepatic triglyceride lipase (HTL) are involved in the hydrolysis of triglycerides of chylomicron (CM) and very low density lipoprotein (VLDL). LL activity and apolipoprotein C Ⅱ (ApoC Ⅱ) have a certain relationship. This article will biochemical and clinical perspective LL deficiency (familial hyperlipoproteinemia type Ⅰ), HTL deficiency and lack of ApoC Ⅱ to explore. Hydrolysis of triglycerides in chylomicrons (CM) and very low density lipoproteins (VLDL) catalyzes at least two enzymes, lipoprotein lipase (LL) and hepatic triglyceride lipase (HTL). They are all glycoproteins, both present in capillary endothelial cells. The main difference between LL and HTL is that complete activation of LL depends on ApoCII. The activity of ApoCII on LL is a complex factor, whereas the activity of HTL