Kovanen P T, Nikkilä E A
Biochim Biophys Acta. 1976 Sep 27;441(3):357-69. doi: 10.1016/0005-2760(76)90233-2.
Isolated rat adipocytes were incubated with serum lipoproteins or lymphchylomicrons which contained 14c-labeled cholesterol. The specific activity of lipoprotein free cholesterol decreased and that of cellular free cholesterol increased linearly up to 7 h. At this time the cell cholesterol specific activity was only 11% of that of medium cholesterol indicating that the rate of exchange was slow. The specific activity of lipoprotein esterified cholesterol remained unchanged while that of cells showed a slight increase suggesting esterification of incorporated free cholesterol. No detectable change of the lipoprotein or cellular cholesterol concentration occurred indicating that the uptake of radioactive free cholesterol was due to exchange without net movement of sterol. The radioactive cholesterol was incorporated into both membrane fraction and the fat droplet of the adipocytes. The rate of cholesterol exchange was temperature-dependent but it was not influenced by the metabolic state of the cells and not by addition of metabolic inhibitors. Trypsin or pronase treatment of the cells were without influence on the rate of the exchange and denaturation of the plasma lipoproteins with formalin increased the rate of exchange. These results indicate that the exchange of cholesterol is a physical chemical process, which is not linked to energy metabolism of the cells, and which is not mediated by either specific lipoprotein receptors on fat cell membranes or pinocytic uptake of lipoproteins. The rate of free cholesterol exchange showed a linear correlation with the concentration of lipoprotein particles in the medium. The relative transfer rate was highest for chylomicrons and decreased in order chylomicron remnants greater than very low density lipoprotein greater than low density lipoprotein greater than high density lipoprotein. A saturation of the system could be obtained only with high density lipoprotein.
将分离出的大鼠脂肪细胞与含有14C标记胆固醇的血清脂蛋白或淋巴乳糜微粒一起孵育。脂蛋白游离胆固醇的比活性降低，而细胞游离胆固醇的比活性在长达7小时内呈线性增加。此时，细胞胆固醇比活性仅为培养基胆固醇比活性的11%，表明交换速率较慢。脂蛋白酯化胆固醇的比活性保持不变，而细胞的比活性略有增加，提示摄入的游离胆固醇发生了酯化。脂蛋白或细胞胆固醇浓度未发生可检测到的变化，表明放射性游离胆固醇的摄取是由于交换，而甾醇没有净移动。放射性胆固醇被整合到脂肪细胞的膜部分和脂肪滴中。胆固醇交换速率与温度有关，但不受细胞代谢状态的影响，也不受代谢抑制剂添加的影响。用胰蛋白酶或链霉蛋白酶处理细胞对交换速率没有影响，用福尔马林使血浆脂蛋白变性会增加交换速率。这些结果表明，胆固醇的交换是一个物理化学过程，与细胞的能量代谢无关，也不是由脂肪细胞膜上的特异性脂蛋白受体或脂蛋白的胞饮摄取介导的。游离胆固醇交换速率与培养基中脂蛋白颗粒的浓度呈线性相关。相对转移速率以乳糜微粒最高，按乳糜微粒残粒＞极低密度脂蛋白＞低密度脂蛋白＞高密度脂蛋白的顺序降低。只有高密度脂蛋白才能使该系统达到饱和。
