Rodriguez J L, Catapano A, Ghiselli G C, Sirtori C R
Center E. Grossi Paoletti for the Study of Metabolic Diseases and Hyperlipidemias, University of Milan, Italy.
Atherosclerosis. 1976 Jan-Feb;23(1):85-96. doi: 10.1016/0021-9150(76)90120-9.
The metabolic fate of very low density lipoproteins (VLDL) in normal and hypercholesteremic (h.c.) rabbits has been investigated. VLDL were labelled with 125I in the protein moieties and injected into normal and h.c. animals. The turnover of h.c. VLDL is markedly delayed as compared to that of normal VLDL, and conversion into lipoprotein classes of higher density is considerably decreased. This is observed when h.c. VLDL are injected either into h.c., or into normal rabbits. Arterial uptake of radioactivity is much higher with h.c. VLDL than with the normal lipoproteins, and it is highest when h.c. VLDL are injected into normal recipients. These data, together with those reported in the previous study, support the hypothesis that h.c. VLDL have an inherent atherogenicity. Injection of h.c. VLDL into normal animals also offers an experimental model for testing drugs or diets against atherosclerosis, using untreated animals.
已对正常和高胆固醇血症(h.c.)兔体内极低密度脂蛋白(VLDL)的代谢命运进行了研究。将蛋白质部分用125I标记的VLDL注入正常和h.c.动物体内。与正常VLDL相比,h.c. VLDL的周转明显延迟,向更高密度脂蛋白类别的转化也显著减少。当将h.c. VLDL注入h.c.兔或正常兔体内时均观察到这一现象。h.c. VLDL的动脉放射性摄取远高于正常脂蛋白,当将h.c. VLDL注入正常受体时摄取最高。这些数据,连同先前研究中报告的数据,支持了h.c. VLDL具有内在致动脉粥样硬化性的假说。将h.c. VLDL注入正常动物体内还为使用未治疗的动物测试抗动脉粥样硬化药物或饮食提供了一个实验模型。