Portman O W, Soltys P, Alexander M, Osuga T
J Lipid Res. 1970 Nov;11(6):596-604.
We have studied the effect of long-term hyperlipemia and atherosclerosis in squirrel monkeys on the metabolism of lysolecithin-(14)C (1-palmitoyl-1'-(14)C sn-glycerol 3-phosphorylcholine) in order to explain elevated plasma and arterial concentrations of lysolecithin. The die-away curves of lysolecithin-(14)C from plasma and the timing of appearances of other (14)C-labeled moieties in plasma and other tissues demonstrated a complex pattern of metabolic reactions. There was a rapid equilibration of specific activities of lysolecithin of plasma, liver, and aortic intima plus inner media. The specific activities of lecithin peaked first in liver, then in plasma, and rose slowly in aortic intima plus inner media. The appearance of lecithin-(14)C in heart and skeletal muscle was also slower than in the liver and some other tissues. Triglycerides, and to a lesser extent, cholesteryl esters contained radioactivity. The concentrations of aortic lysolecithin in the atherosclerotic aortas were several times greater than comparable values for control aortas, and the time of equilibration of plasma and aorta lysolecithin-(14)C was much greater for the atherosclerotic group. The quantities of lysolecithin in plasma and in the pool of which the plasma was a part, were increased with hyperlipemia and atherosclerosis, as was the rate of lysolecithin production in the fast pool. Hyperlipemia was also associated with an early increase in plasma lecithin:cholesterol acyltransferase (LCAT) activity in vitro. Furthermore, nutritional hyperlipemia influenced the distribution of lysolecithin-(14)C and lecithin-(14)C between different plasma lipoproteins. The increase in concentrations of lysolecithin in the aorta occurred more slowly than that in plasma after we had induced hyperlipemia in the monkeys.
我们研究了松鼠猴长期高脂血症和动脉粥样硬化对溶血卵磷脂 -（14）C（1 - 棕榈酰 - 1'-（14）C - sn - 甘油 - 3 - 磷酸胆碱）代谢的影响，以解释血浆和动脉中溶血卵磷脂浓度升高的原因。血浆中溶血卵磷脂 -（14）C的消失曲线以及血浆和其他组织中其他（14）C标记部分出现的时间表明了代谢反应的复杂模式。血浆、肝脏和主动脉内膜加中膜的溶血卵磷脂比活性迅速达到平衡。卵磷脂的比活性首先在肝脏中达到峰值，然后在血浆中达到峰值，并在主动脉内膜加中膜中缓慢上升。心脏和骨骼肌中卵磷脂 -（14）C的出现也比肝脏和其他一些组织慢。甘油三酯以及程度较轻的胆固醇酯含有放射性。动脉粥样硬化主动脉中的主动脉溶血卵磷脂浓度比对照主动脉的可比值高几倍，并且动脉粥样硬化组血浆和主动脉溶血卵磷脂 -（14）C达到平衡的时间长得多。高脂血症和动脉粥样硬化会使血浆中溶血卵磷脂的含量以及血浆所属池中的溶血卵磷脂含量增加，快速池中溶血卵磷脂的产生速率也会增加。高脂血症还与体外血浆卵磷脂：胆固醇酰基转移酶（LCAT）活性的早期增加有关。此外，营养性高脂血症影响了溶血卵磷脂 -（14）C和卵磷脂 -（14）C在不同血浆脂蛋白之间的分布。在我们诱导猴子出现高脂血症后，主动脉中溶血卵磷脂浓度的增加比血浆中溶血卵磷脂浓度的增加要慢。
