Vega G L, Grundy S M
Center for Human Nutrition, University of Texas Southwestern Medical Center, Dallas 75235-9052.
Arterioscler Thromb. 1993 Apr;13(4):579-89. doi: 10.1161/01.atv.13.4.579.
The objective of this study was to determine whether normotriglyceridemic patients with low levels of high density lipoprotein (HDL) cholesterol have concomitant defects in the metabolism of low density lipoproteins (LDLs). To address this question, measurements of turnover rates of apolipoprotein A-I (apo A-I) and LDL apolipoprotein B (apo B) were made in 36 middle-aged men with low HDL cholesterol (< 40 mg/dL), normal triglyceride (< 250 mg/dL), and normal total cholesterol (< or = 90th percentile) levels. Similar measurements were made in eight hypertriglyceridemic men having low HDL levels. For control, turnover rates of LDL apo B were measured in 24 healthy, normolipidemic men, and apo A-I kinetics were determined in 20 other healthy men with normal HDL cholesterol levels. In all patients with low HDL levels, fractional catabolic rates (FCRs) for apo A-I were increased compared with control subjects; in contrast, input rates for apo A-I in low-HDL patients were similar to control. Hypertriglyceridemic patients had significantly higher FCRs for LDL (0.463 +/- 0.040 pool/day, [mean +/- SEM]) than control subjects (0.328 +/- 0.008 pool/day, p < 0.001). In normolipidemic patients having low HDL, a bimodal pattern of LDL-apo B kinetics was observed. For 23 low-HDL patients, FCRs for LDL apo B averaged 0.450 +/- 0.017 pool/day and were significantly higher than control values. Additionally, in these patients, levels of very low density lipoprotein plus intermediate density lipoprotein (VLDL+IDL) cholesterol and VLDL+IDL apo B were higher than in control subjects (54 +/- 3 versus 32 +/- 3 mg/dL and 25 +/- 2 versus 18 +/- 1 mg/dL, respectively). The remaining 13 low-HDL patients had lower and essentially normal FCRs for LDL (0.300 +/- 0.009 pool/day); these patients also had relatively low levels of cholesterol and apo B in VLDL+IDL. Thus, two patterns of LDL kinetics were present in normotriglyceridemic patients with low HDL levels. One pattern was indistinguishable from that typically present in patients with hypertriglyceridemia, whereas the other was similar to normal control subjects. These two patterns of LDL-apo B kinetics may reflect different mechanisms for the causation of low HDL cholesterol concentrations.
本研究的目的是确定高密度脂蛋白（HDL）胆固醇水平低的正常甘油三酯血症患者是否同时存在低密度脂蛋白（LDL）代谢缺陷。为解决这个问题，对36名HDL胆固醇水平低（<40mg/dL）、甘油三酯正常（<250mg/dL）且总胆固醇正常（<或=第90百分位数）水平的中年男性进行了载脂蛋白A-I（apo A-I）和LDL载脂蛋白B（apo B）转换率的测量。对8名HDL水平低的高甘油三酯血症男性进行了类似测量。作为对照，对24名健康、血脂正常的男性测量了LDL apo B的转换率，并对另外20名HDL胆固醇水平正常的健康男性测定了apo A-I动力学。在所有HDL水平低的患者中，apo A-I的分解代谢分数率（FCRs）与对照受试者相比有所增加；相比之下，HDL水平低的患者中apo A-I的输入率与对照相似。高甘油三酯血症患者的LDL的FCRs（0.463±0.040池/天，[平均值±标准误]）显著高于对照受试者（0.328±0.008池/天，p<0.001）。在HDL水平低的血脂正常患者中，观察到LDL-apo B动力学的双峰模式。对于23名HDL水平低的患者，LDL apo B的FCRs平均为0.450±0.017池/天，显著高于对照值。此外，在这些患者中，极低密度脂蛋白加中间密度脂蛋白（VLDL+IDL）胆固醇和VLDL+IDL apo B的水平高于对照受试者（分别为54±3对32±3mg/dL和25±2对18±1mg/dL）。其余13名HDL水平低的患者LDL的FCRs较低且基本正常（0.300±0.009池/天）；这些患者VLDL+IDL中的胆固醇和apo B水平也相对较低。因此，HDL水平低的正常甘油三酯血症患者存在两种LDL动力学模式。一种模式与高甘油三酯血症患者中典型存在的模式无法区分，而另一种模式与正常对照受试者相似。这两种LDL-apo B动力学模式可能反映了HDL胆固醇浓度降低的不同致病机制。
