Martins I J, Redgrave T G
Department of Physiology, University of Western Australia, Nedlands.
Biochem J. 1992 Feb 1;281 ( Pt 3)(Pt 3):851-7. doi: 10.1042/bj2810851.
Triolein/cholesteryl oleate/cholesterol/phosphatidylcholine emulsions designed to model the lipid composition of chylomicrons were injected intravenously into control and streptozotocin-treated insulin-deficient rats. As previously described for lymph chylomicrons, the emulsion triolein was hydrolysed and phosphatidylcholine was transferred to the plasma high-density lipoproteins (HDL). This mechanism was used to introduce a phospholipid label into HDL in vivo. The subsequent clearance of phospholipid radioactivity from the plasma of insulin-deficient rats was significantly slower than in controls (P less than 0.025). Plasma clearance was similarly slower in insulin-deficient rats after injection of HDL that was previously labelled with radioactive phospholipids. After injection, the phospholipid label redistributed rapidly between the large-particle fraction of plasma lipoproteins (very-low- and low-density lipoproteins), and the lighter and heavier fractions of HDL. Compared with control rats, in insulin-deficient rats less of the phospholipid label was distributed to the lighter HDL fraction and more to the heavier HDL fraction, and this difference was not due to changes in activity of lecithin: cholesterol acyltransferase or in the apparent activity of phospholipid transfer protein. In insulin-deficient rats the changes in HDL phospholipid clearance and exchange appeared to be secondary to the associated hypertriglyceridaemia and the related changes in distribution of phospholipids between classes of plasma lipoproteins.
旨在模拟乳糜微粒脂质组成的三油酸甘油酯/胆固醇油酸酯/胆固醇/磷脂酰胆碱乳剂,经静脉注射到对照大鼠和经链脲佐菌素处理的胰岛素缺乏大鼠体内。正如先前对淋巴乳糜微粒的描述,乳剂中的三油酸甘油酯被水解,磷脂酰胆碱转移到血浆高密度脂蛋白(HDL)中。利用这一机制在体内将磷脂标记引入HDL。胰岛素缺乏大鼠血浆中磷脂放射性的后续清除明显慢于对照大鼠(P小于0.025)。注射预先用放射性磷脂标记的HDL后,胰岛素缺乏大鼠的血浆清除同样较慢。注射后,磷脂标记在血浆脂蛋白的大颗粒部分(极低密度和低密度脂蛋白)以及HDL的较轻和较重部分之间迅速重新分布。与对照大鼠相比,在胰岛素缺乏大鼠中,较少的磷脂标记分布到较轻的HDL部分,较多分布到较重的HDL部分,且这种差异并非由于卵磷脂胆固醇酰基转移酶活性或磷脂转移蛋白的表观活性变化所致。在胰岛素缺乏大鼠中,HDL磷脂清除和交换的变化似乎继发于相关的高甘油三酯血症以及血浆脂蛋白类别之间磷脂分布的相关变化。