HDL content and composition in acute phase response in three species: triglyceride enrichment of HDL a factor in its decrease.

HDL content and composition in acute phase response in three species: triglyceride enrichment of HDL a factor in its decrease.
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DOI:
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发表时间:
1996-12
影响因子:
6.5
通讯作者:
Veneracion;Cabana;J. Lukens;K. Rice;Terry J. Hawkins;G. Getz
Veneracion;Cabana;J. Lukens;K. Rice;Terry J. Hawkins;G. Getz
中科院分区:
生物学2区
文献类型:
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作者:
Veneracion;Cabana;J. Lukens;K. Rice;Terry J. Hawkins;G. Getz

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高密度脂蛋白(HDL)水平在急性期反应(APR)期间降低。本研究采用家兔、狒狒和小鼠的APR模型,研究影响HDL水平的因素。在狒狒和家兔中,存在大量高脂血症、HDL的甘油三酯富集(核心脂质的60-80%)、HDL-胆固醇和载脂蛋白(apo)A-I降低(至基线的10%)以及非脂蛋白底部组分中apoA-I升高,表明apoA-I与颗粒分离。在兔子中进行的富含血清淀粉样蛋白A(SAA)的HDL的详细分析揭示了含有> 95%SAA的大的、富含磷脂酰胆碱(> 60%的核心脂质)的颗粒。这些颗粒具有高的表核比(13.4 +/- 1.94,对照= 3.0 +/- 0.12)和非常高的蛋白质(79.71 +/- 5.25重量%,对照= 37.2 +/- 0.43)比例,当通过非变性梯度电泳检查时,大(r = 5.95 nm),但当通过电子显微镜检查时,小(r = 4.2 nm)。在小鼠中,没有高甘油三酯血症,没有HDL的甘油三酯富集,没有HDL胆固醇降低。ApoA-I降低至基线的约61.4%,但在底部部分中没有增加,尽管也产生了大但致密的SAA富集的HDL颗粒。这些结果表明,hyperglycidemia,甘油三酯富集的HDL,和apoA-I的颗粒的解离,可能由SAA的apoA-I的位移,是重要的因素,在下降的HDL在APR期间。是否甘油三酯代谢的差异占HDL反应的差异,在研究的物种需要进一步的实验。
High density lipoprotein (HDL) levels decrease during the acute phase response (APR). We have used the APR model of rabbit, baboon, and mouse to study the factors that influence HDL level. In the baboons and rabbits there was massive hypertriglyceridemia, triglyceride enrichment of HDL (60-80% of core lipids), decreases of HDL-cholesterol and apolipoprotein (apo)A-I (to 10% of baseline), and increases of apoA-I in the non-lipoprotein bottom fraction suggesting dissociation of apoA-I from the particles. Detailed analyses of serum amyloid A (SAA)-rich HDL done in the rabbit revealed large, triglyceride-enriched (> 60% of core lipids) particles containing > 95% SAA. These particles had a high surface to core ratio (13.4 +/- 1.94, control = 3.0 +/- 0.12) and a very high protein (79.71 +/- 5.25 weight %, control = 37.2 +/- 0.43) proportion, large (r = 5.95 nm) when examined by non-denaturing gradient electrophoresis but small when examined by electron microscopy (r = 4.2 nm). In the mouse there was no hypertriglyceridemia, no triglyceride enrichment of HDL, no decrease of HDL cholesterol. ApoA-I decreased to about 61.4% of baseline but did not increase in the bottom fraction although large but dense SAA-enriched HDL particles were also produced. These results suggest that hypertriglyceridemia, triglyceride-enrichment of HDL, and dissociation of apoA-I from the particles, possibly by displacement of apoA-I by SAA, are important factors in the decline of HDL during the APR. Whether differences in triglyceride metabolism account for the differences in the HDL response in the species studied requires further experimentation.