Metabolic relationships among the plasma lipoproteins. Reciprocal changes in the concentrations of very low and low density lipoproteins in man.
Metabolic relationships among the plasma lipoproteins. Reciprocal changes in the concentrations of very low and low density lipoproteins in man.
复制标题
血浆脂蛋白之间的代谢关系。
DOI：
10.1172/jci106896
复制
发表时间：
1972
期刊：
影响因子：
--
通讯作者：
R. Lees
中科院分区：
文献类型：
--
作者：
D. Wilson;R. Lees
研究了31名正常和高脂血症男性和女性在减肥、碳水化合物诱导或氯贝特治疗后，伴随极低密度脂蛋白(VLDL)变化的其他血浆脂蛋白的变化。在对照组和治疗期间连续测量血脂和个体脂蛋白胆固醇浓度。采用放射免疫扩散法检测低密度脂蛋白(LDL)。随着三种代谢紊乱的出现，极低密度脂蛋白和低密度脂蛋白发生了相反方向的变化。高密度脂蛋白(高密度脂蛋白)胆固醇的变化与低密度脂蛋白的变化大致相似，但不太一致。两名III型高脂蛋白血症患者在减肥或氯贝特治疗后，尽管血浆甘油三酯或极低密度脂蛋白降低了40%以上，但未能显示出低密度脂蛋白的对等增加。在氯贝特治疗后，低密度脂蛋白的增加与治疗期间极低密度脂蛋白胆固醇的绝对下降成比例。与低密度脂蛋白相比，低密度脂蛋白变化相对较小。血浆极低密度脂蛋白和低密度脂蛋白浓度长期相互依赖的机制尚不清楚，可能是这些脂蛋白相互转化的速率改变的结果，或者是极低密度脂蛋白对低密度脂蛋白产生和释放的反馈抑制所致。
The changes in other plasma lipoproteins which accompany alterations in very low density lipoproteins (VLDL) were studied in 31 normal and hyperlipidemic men and women who underwent weight reduction, carbohydrate induction, or clofibrate treatment. Plasma lipids and individual lipoprotein cholesterol concentrations were measured serially during control and treatment periods. Low density lipoprotein (LDL) protein was determined by radial immunodiffusion. Oppositely directed changes in VLDL and LDL were found with each of the three metabolic perturbations. Changes in high density lipoprotein (HDL) cholesterol generally paralleled those in LDL but were less consistent. Two patients with type III hyperlipoproteinemia failed to demonstrate reciprocal increases in LDL despite more than 40% reduction in plasma glycerides or VLDL with weight reduction or clofibrate therapy. After clofibrate therapy, LDL increased in proportion to the absolute decrease in VLDL cholesterol during treatment. LDL protein changed relatively less than did LDL cholesterol. The mechanism for the interdependency of plasma VLDL and LDL concentrations over the long term is not known and may be the result of altered rates of interconversion of these lipoproteins, or to feedback inhibition by VLDL of LDL production and release.