INCREASED APO-A-I AND APO-A-II FRACTIONAL CATABOLIC RATE IN PATIENTS WITH LOW HIGH-DENSITY LIPOPROTEIN-CHOLESTEROL LEVELS WITH OR WITHOUT HYPERTRIGLYCERIDEMIA
INCREASED APO-A-I AND APO-A-II FRACTIONAL CATABOLIC RATE IN PATIENTS WITH LOW HIGH-DENSITY LIPOPROTEIN-CHOLESTEROL LEVELS WITH OR WITHOUT HYPERTRIGLYCERIDEMIA
复制标题
DOI：
10.1172/jci115028
复制
发表时间：
1991-02-01
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
低密度脂蛋白胆固醇(HDLC)水平可能会增加动脉粥样硬化的风险，并经常与高甘油三酯血症(HTG)相关；然而，无论有没有HTG，低HDLC水平的代谢原因都鲜为人知。本文研究了15例低密度脂蛋白胆固醇、6例正常血浆甘油三酯和9例高甘油三酯受试者的放射性高密度脂蛋白-载脂蛋白A-I和载脂蛋白A-II的代谢，并与13例正常的正常受试者进行了比较。两组载脂蛋白A-I的部分分解代谢率(0.313+/-0.052和0.323+/-0.063对0.245+/-0.036和0.239+/-0.037对0.185+/-0.185+/-0.031pos/d)均高于第3组(P=0.006)。因此，无论有无HTG，高FCR都表现为低高密度脂蛋白胆固醇。载脂蛋白A-I的转运速率(Tr)在两组间无显著差异，而载脂蛋白A-Ⅱ的转运速率仅在2组和3组之间有差异(分别为2.15±0.57、2.50±0.39和1.83+/-0.48 mg/kg/d，P=0.016)。高密度脂蛋白相关因素在第1组和第2组相似，但在第3组不同，如FCR，包括肝素后血浆脂蛋白脂肪酶与肝脂酶活性的比率(LPL/HL)，高密度脂蛋白-C与载脂蛋白A-I加载脂蛋白A-II的比率，以及示踪剂在D>中的百分比(两者均为0.74，P<；0.0001)。与FCR相关的主要因素是高密度脂蛋白胆固醇/载脂蛋白A-I+载脂蛋白A-II、LPL/HL和血浆甘油三酯水平。我们推测脂肪酶活性和血浆甘油三酯影响高密度脂蛋白组成，高密度脂蛋白组成调节低密度脂蛋白胆固醇，高密度脂蛋白调节高密度脂蛋白胆固醇。因此，HTG只是可能导致FCR升高和低HDL-C的几个因素之一。考虑到高密度脂蛋白组成改变与高FCR和低高密度脂蛋白胆固醇水平的关系，影响高密度脂蛋白组成的因素可能增加动脉粥样硬化的易感性。
Low HDL-cholesterol (HDL-C) levels may elevate atherosclerosis risk, and often associate with hypertriglyceridemia (HTG); however, the metabolic causes of low HDL-C levels with or without HTG are poorly understood. We studied the turnover of radioiodinated HDL apolipoproteins, apo A-I and apo A-II, in 15 human subjects with low HDL-C, six with normal plasma TG levels (group 1) and nine with high TG (group 2), and compared them to 13 control subjects with normal HDL-C and TG levels (group 3). The fractional catabolic rate (FCR) was equally elevated in groups 1 and 2 vs. group 3 for both apo A-I (0.313 +/- 0.052 and 0.323 +/- 0.063 vs. 0.245 +/- 0.036 and 0.239 +/- 0.037 vs 0.185 +/- 0.185 +/- 0.031 pools/d, P = 0.006). Thus, high FCR characterized low HDL-C regardless of the presence or absence of HTG. In contras, transport rate (TR) of apo A-I did not differ significantly among the groups and the apo A-II TR differed only between groups 2 and 3 (2.15 +/- 0.57, 2.50 +/- 0.39, and 1.83 +/- 0.48 mg/kg per d for groups 1 to 3, respectively, P = 0.016. Several HDL-related factors were similar in groups 1 and 2 but differed in group 3, as with FCR, including the ratio of lipoprotein lipase to hepatic lipase activity (LPL/HL) in post-heparin plasma, the ratio of the HDL-C to apo A-I plus apo A-II levels, and the percent of tracer in the D > 0.74, P < 0.0001 for both). Major correlates of FCR were HDL-C/apo A-I + apo A-II, LPL/HL, and plasma TG levels.We hypothesize the lipase activity and plasma TG affect HDL composition which modulates FCR, which in turn regulates HDL-C. Thus, HTG is only one of several factors which may contribute to elevated FCR and low HDL-C. Given the relationship of altered HDL composition with high FCR and low HDL-C levels, factors affecting HDL composition may increase atherosclerosis susceptibility.