ELEVATED HIGH-DENSITY LIPOPROTEIN CHOLESTEROL LEVELS CORRELATE WITH DECREASED APOLIPOPROTEIN-A-I AND APOLIPOPROTEIN-A-II FRACTIONAL CATABOLIC RATE IN WOMEN
ELEVATED HIGH-DENSITY LIPOPROTEIN CHOLESTEROL LEVELS CORRELATE WITH DECREASED APOLIPOPROTEIN-A-I AND APOLIPOPROTEIN-A-II FRACTIONAL CATABOLIC RATE IN WOMEN
复制标题
DOI：
10.1172/jci114149
复制
发表时间：
1989-07-01
影响因子：
15.9
通讯作者：
BRESLOW, JL
中科院分区：
文献类型：
--
作者：
BRINTON, EA;EISENBERG, S;BRESLOW, JL
高水平的HDL-胆固醇（HDL-C）可预防冠心病易感性，但HDL-C水平升高的代谢机制尚不清楚。我们现在报告的营业额的同位素放射性碘标记的HDL载脂蛋白，载脂蛋白A-I和载脂蛋白A-II，在15名女性受试者的代谢饮食与HDL-C水平范围从51至122毫克/分升。测定所有受试者的apo A-I和apo A-II代谢参数，即分解率（FCR）和绝对合成率（SR）。血浆HDL-C与apoA-I和apoA-II的FCR呈负相关（r分别为-0.75，P < 0.001和-0.54，P = 0.036），与apoA-I和apoA-II的SR无相关性（r分别为-0.09，r =-0.16，P = NS）。载脂蛋白A-I水平与载脂蛋白A-I FCR呈负相关（r=-0.64，P = 0.01），但与载脂蛋白A-I SR无相关性（r= 0.30，P = NS）。血浆apo A-II水平与apo A-II FCR无相关性（r=-0.38，P = 0.16），但与apo A-II SR相关（r= 0.65，P = 0.009）。进一步分析显示，apo A-I和apo A-II FCR与HDL-C/apo A-I + A-II比值呈负相关（r分别为-0.69和-0.61，P = 0.005和0.015）。这些数据表明：（a）低HDL载脂蛋白FCR是升高的HDL-C水平的主要代谢机制;（B）apo A-I FCR是控制血浆apo A-I水平的主要因素，但apo A-II SR是控制血浆apo A-II水平的主要因素;（c）低HDL载脂蛋白FCR与富含脂质的HDL组分相关。这些发现阐明了HDL代谢的各个方面，这些方面有助于高HDL-C水平，并可能构成对冠心病的保护机制。
High levels of HDL-cholesterol (HDL-C) protect against coronary heart disease susceptibility, but the metabolic mechanisms underlying elevated HDL-C levels are poorly understood. We now report the turnover of isologous radioiodinated HDL apolipoproteins, apo A-I and apo A-II, in 15 female subjects on a metabolic diet with HDL-C levels ranging from 51 to 122 mg/dl. The metabolic parameters, fractional catabolic rate (FCR) and absolute synthetic rate (SR), were determined for apo A-I and apo A-II in all subjects. There was an inverse correlation between plasma HDL-C and the FCR of apo A-I and apo A-II (r = -0.75, P < 0.001, and 4= -0.54, P = 0.036, respectively), but no correlation with the SR of either apo A-I or apo A-II (r = -0.09, and r= - 0.16, respectively, both P = NS). Apo A-I levels correlated inversely with apo A-I FCR (r= -0.64, P = 0.01) but not with apo A-I SR (r= 0.30, P = NS). In contrast, plasma levels of apo A-II did not correlate with apo A-II FCR (r= -0.38, P = 0.16), but did correlate with apo A-II SR (r= 0.65, P = 0.009). Further analysis showed that apo A-I and apo A-II FCR were inversely correlated with the HDL-C/apo A-I + A-II ratio (r= -0.69 and -0.61, P = 0.005 and 0.015, respectively). These data suggest that: (a) low HDL apolipoprotein FCR is the predominant metabolic mechanism of elevated HDL-C levels; (b) apo A-I FCR is the primary factor in controlling plasma apo A-I levels, but apo A-II SR is the primary factor controlling plasma apo A-II levels; (c) low HDL apolipoprotein FCR is associated with a lipid-rich HDL fraction. These findings elucidate aspects of HDL metabolism which contribute to high HDL-C levels and which may constitute mechanisms for protection against coronary heart disease.