Sauar J, Ritland S, Holme R, Horn R
Clin Chim Acta. 1978 Sep 15;88(3):461-7. doi: 10.1016/0009-8981(78)90281-4.
Lipoprotein-X containing plasma from a patient with familial lecithin:cholesterol acyltransferase (LCAT) deficiency, was used as substrate and incubated with postheparin plasma or partly purified lipases. LP-X could not be demonstrated by agar gel electrophoresis after incubation with postheparin plasma from a healthy subject, from a patient with chronic active hepatitis deficient in hepatic lipase, or with partly purified lipoprotein lipase. After incubation a marked increase in free fatty acids (FFA) was observed. In contrast LP-X was still present after incubation when postheparin plasma deficient in lipoprotein lipase or partly purified hepatic lipase was added to the substrate. Only minor changes in the concentration of FFA occurred. After addition of oleic acid to the substrate LP-X could not be demonstrated by agar gel electrophoresis. However, in the isolated low density lipoproteins, LP-X like particles were still present as viewed by electron microscopy. Our results strongly suggest that the change in electrophoretic mobility of LP-X was induced by the release of FFA. This was achieved by lipoprotein lipase, but not by hepatic lipase.
胆固醇酰基转移酶（LCAT）缺乏症患者的含脂蛋白-X血浆被用作底物，并与肝素后血浆或部分纯化的脂肪酶一起孵育。与健康受试者、缺乏肝脂肪酶的慢性活动性肝炎患者的肝素后血浆或部分纯化的脂蛋白脂肪酶孵育后，琼脂凝胶电泳未显示出脂蛋白-X。孵育后观察到游离脂肪酸（FFA）显著增加。相比之下，当将缺乏脂蛋白脂肪酶的肝素后血浆或部分纯化的肝脂肪酶添加到底物中进行孵育时，脂蛋白-X仍然存在。游离脂肪酸浓度仅发生轻微变化。向底物中添加油酸后，琼脂凝胶电泳未显示出脂蛋白-X。然而，通过电子显微镜观察，在分离的低密度脂蛋白中，仍存在类似脂蛋白-X的颗粒。我们的结果强烈表明，脂蛋白-X电泳迁移率的变化是由游离脂肪酸的释放引起的。这是由脂蛋白脂肪酶实现的，而不是由肝脂肪酶实现的。
