Liu B W, Hynd B A, Kashyap M L
Biochem Biophys Res Commun. 1984 Jun 29;121(3):946-52. doi: 10.1016/0006-291x(84)90768-x.
Lipolysis of human very low density lipoproteins (VLDL) by lipoprotein lipase (LPL) was inhibited in the presence of high density lipoproteins (HDL), anti-apolipoprotein (apo) CII, and by increasing the VLDL free cholesterol content but not with anti-apo CIII or lipoprotein-free plasma. The experiments lend direct evidence that the composition of VLDL and their milieu are important determinants of lipolysis by LPL. Apo CIII may not be critical in LPL mediated VLDL catabolism.
在存在高密度脂蛋白(HDL)、抗载脂蛋白(apo)CII以及增加极低密度脂蛋白(VLDL)游离胆固醇含量的情况下,脂蛋白脂肪酶(LPL)对人极低密度脂蛋白(VLDL)的脂解作用受到抑制,但抗apo CIII或无脂蛋白血浆不会产生这种抑制作用。这些实验提供了直接证据,表明VLDL的组成及其周围环境是LPL介导脂解作用的重要决定因素。Apo CIII在LPL介导的VLDL分解代谢中可能并不关键。