Sammett D, Tall A R
J Biol Chem. 1985 Jun 10;260(11):6687-97.
Lipoprotein lipase enhances the cholesteryl ester transfer protein (CETP)-mediated transfer of cholesteryl esters from plasma high density lipoproteins (HDL) to very low density lipoproteins (VLDL). In time course studies the stimulation of cholesteryl ester transfer by bovine milk lipase was correlated with accumulation of fatty acids in VLDL remnants. As the amount of fatty acid-poor albumin in the incubations was increased, there was decreased accumulation of fatty acids in VLDL remnants and a parallel decrease in the stimulation of cholesteryl ester transfer by lipolysis. Addition of sodium oleate to VLDL and albumin resulted in stimulation of the CETP-mediated transfer of cholesteryl esters from HDL to VLDL. The stimulation of transfer of cholesteryl esters into previously lipolyzed VLDL was abolished by lowering the pH from 7.5 to 6.0, consistent with a role of lipoprotein ionized fatty acids. CETP-mediated cholesteryl ester transfer from HDL to VLDL was also augmented by phosholipase A2 and by a bacterial lipase which lacked phospholipase activity. When VLDL and HDL were re-isolated after a lipolysis experiment, both lipoproteins stimulated CETP activity. Postlipolysis VLDL and HDL bound much more CETP than native VLDL or HDL. Lipolysis of apoprotein-free phospholipid/triglyceride emulsions also resulted in enhanced binding of CETP to the emulsion particles. Incubation conditions which abolished the enhanced cholesteryl ester transfer into VLDL remnants reduced binding of CETP to remnants, emulsions, and HDL. In conclusion, the enhanced CETP-mediated transfer of cholesteryl esters from HDL to VLDL during lipolysis is related to the accumulation of products of lipolysis, especially fatty acids, in the lipoproteins. Lipids accumulating in VLDL remnants and HDL as a result of lipolysis may augment binding of CETP to these lipoproteins, leading to more efficient transfer of cholesteryl esters from HDL to VLDL.
脂蛋白脂肪酶可增强胆固醇酯转运蛋白（CETP）介导的胆固醇酯从血浆高密度脂蛋白（HDL）向极低密度脂蛋白（VLDL）的转运。在时间进程研究中，牛乳脂肪酶对胆固醇酯转运的刺激作用与VLDL残粒中脂肪酸的积累相关。随着孵育体系中脂肪酸缺乏白蛋白量的增加，VLDL残粒中脂肪酸的积累减少，同时脂解作用对胆固醇酯转运的刺激作用也相应降低。向VLDL和白蛋白中添加油酸钠可刺激CETP介导的胆固醇酯从HDL向VLDL的转运。将pH从7.5降至6.0可消除胆固醇酯向先前已脂解的VLDL的转运刺激作用，这与脂蛋白离子化脂肪酸的作用一致。磷脂酶A2和一种缺乏磷脂酶活性的细菌脂肪酶也可增强CETP介导的胆固醇酯从HDL向VLDL的转运。脂解实验后重新分离VLDL和HDL时，两种脂蛋白均刺激CETP活性。脂解后的VLDL和HDL比天然VLDL或HDL结合更多的CETP。无载脂蛋白的磷脂/甘油三酯乳剂的脂解也导致CETP与乳剂颗粒的结合增强。消除胆固醇酯向VLDL残粒转运增强的孵育条件会降低CETP与残粒、乳剂和HDL的结合。总之，脂解过程中CETP介导的胆固醇酯从HDL向VLDL的转运增强与脂解产物尤其是脂肪酸在脂蛋白中的积累有关。脂解导致VLDL残粒和HDL中积累的脂质可能会增强CETP与这些脂蛋白的结合，从而使胆固醇酯从HDL向VLDL的转运更高效。
