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免疫阻断脂解作用导致的血浆脂蛋白变化

Plasma lipoprotein changes resulting from immunologically blocked lipolysis.

作者信息

Behr S R, Patsch J R, Forte T, Bensadoun A

出版信息

J Lipid Res. 1981 Mar;22(3):443-51.

PMID:7240969
Abstract

The role of lipoprotein lipase (LPL) in the generation of low density lipoprotein (LDL) and high density lipoprotein (HDL) was investigated. Intravenous injections of high titer goat antiserum against highly purified chicken LPL into fasted roosters quantitatively blocks the removal of plasma VLDL triglyceride (1976. J. Lipid Res. 17: 498-505). Analyses of the chemical components of lipoproteins after 8 hr of LPL inhibition showed that the very low density lipoprotein (VLDL) concentration increased over 10-fold, while LDL and HDL concentrations decreased by 5-fold and 48%, respectively. LDL and HDL cholesterol levels decreased logarithmically over the 8-hr period, with half-lives of 2.4 and 6 hr, respectively. The composition of these lipoprotein fractions on a percent weight basis changed significantly. Experimental LDL contained 37% less phospholipid, 64% less cholesterol, and 2.3-fold more triglyceride than control LDL. Experimental HDL contained 3.1-fold more triglyceride and 50% less unesterified cholesterol than control HDL. The Stokes' radii of HDL were determined by gel filtration on Biogel A5M and Ultrogel AcA 22: the radius of experimental HDL (44.9 A) was smaller than that of control HDL (55.4 A). These measurements were confirmed by electron microscopy (43 and 54 A, respectively). After rate zonal ultracentrifugations of plasma samples, control LDL was clearly resolved, while no LDL could be detected in the experimental samples. Rate zonal ultracentrifugations of plasma samples also indicated that control HDL had a higher flotation rate than experimental HDL. Equilibrium zonal ultracentrifugation showed experimental HDL to be more dense than control HDL with hydrated densities of 1.118 and 1.113 g/ml, respectively. These experiments provide in vivo evidence that LDL is a direct metabolic product of VLDL and that LPL plays a role in the transfer of surface constituents from VLDL to HDL.-Behr, S. R., J. R. Patsch, T. Forte, and A. Bensadoun. Plasma lipoprotein changes resulting from immunologically blocked lipolysis.

摘要

研究了脂蛋白脂肪酶(LPL)在低密度脂蛋白(LDL)和高密度脂蛋白(HDL)生成中的作用。向禁食的公鸡静脉注射高滴度的抗高度纯化鸡LPL的山羊抗血清,定量阻断了血浆极低密度脂蛋白(VLDL)甘油三酯的清除(1976年。《脂质研究杂志》17:498 - 505)。LPL抑制8小时后对脂蛋白化学成分的分析表明,极低密度脂蛋白(VLDL)浓度增加了10倍以上,而LDL和HDL浓度分别下降了5倍和48%。在8小时期间,LDL和HDL胆固醇水平呈对数下降,半衰期分别为2.4小时和6小时。这些脂蛋白组分按重量百分比计的组成发生了显著变化。实验性LDL的磷脂含量比对照LDL少37%,胆固醇含量少64%,甘油三酯含量多2.3倍。实验性HDL的甘油三酯含量比对照HDL多3.1倍,未酯化胆固醇含量少50%。HDL的斯托克斯半径通过在Biogel A5M和Ultrogel AcA 22上的凝胶过滤测定:实验性HDL的半径(44.9 Å)小于对照HDL的半径(55.4 Å)。这些测量结果通过电子显微镜得到证实(分别为43 Å和54 Å)。对血浆样品进行速率区带超速离心后,对照LDL清晰可辨,而在实验样品中未检测到LDL。血浆样品的速率区带超速离心还表明,对照HDL的漂浮率高于实验性HDL。平衡区带超速离心显示,实验性HDL比对照HDL密度更大,水合密度分别为1.118和1.113 g/ml。这些实验提供了体内证据,表明LDL是VLDL的直接代谢产物,且LPL在将表面成分从VLDL转移到HDL中起作用。- 贝赫,S.R.,J.R.帕奇,T.福尔特,和A.本萨杜恩。免疫阻断脂解导致的血浆脂蛋白变化。

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