The metabolism of apolipoprotein B in subjects with hypertriglyceridemia and polydisperse LDL.

The metabolism of apolipoprotein B in subjects with hypertriglyceridemia and polydisperse LDL.
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高甘油三酯血症和多分散低密度脂蛋白受试者中载脂蛋白 B 的代谢。

DOI:
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发表时间:
1980
影响因子:
6.5
通讯作者:
M. Berman
M. Berman
中科院分区:
生物学2区
文献类型:
--
作者:
W. Fisher;L. Zech;P. Bardalaye;G. Warmke;M. Berman

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本研究关注多分散性或异质性LDL高脂血症患者的载脂蛋白B(apoB)代谢。5名受试者保持恒定的饮食控制血液样本分馏成极低密度脂蛋白(VLDL),Sf 20,Sf 10,和Sf 4 LDL,和血浆游离亮氨酸,并在3名受试者VLDL进一步细分的大小。分离载脂蛋白B,并测量血浆载脂蛋白B池的质量。注射[3 H]亮氨酸作为代谢示踪剂后,在7或14天内测量这些脂蛋白中载脂蛋白B和血浆亮氨酸的比活性。使用多房室分析检查动力学数据,并根据我们以前的载脂蛋白B代谢模型(1975年)进行解释。24:2263)。新合成的载脂蛋白B以大VLDL的形式分泌,通过脱脂链代谢,产生由小VLDL和Sf 20 LDL组成的中密度脂蛋白(IDL),并最终形成小Sf 4 LDL。低密度脂蛋白(LDL)的代谢是一个从Sf 20到Sf 10和Sf 4LDL的阶梯式过程.载脂蛋白B的第二个主要生物合成输入直接进入IDL,1/4至2/3的新合成载脂蛋白B通过该途径进入血浆。这些受试者的总载脂蛋白B合成是正常人的5- 10倍。VLDL载脂蛋白B和IDL的转运速率比正常情况下慢,停留时间增加约2倍;然而,VLDL载脂蛋白B池扩大了5- 10倍,因此每小时进出该池的载脂蛋白B量远大于正常情况。载脂蛋白B催化剂有两种主要途径。1/3至2/3的载脂蛋白B通过LDL代谢,以Sf 4 LDL形式从血浆中消失。载脂蛋白B的剩余部分直接从血浆IDL中消失。在多分散性LDL高脂血症受试者中apo B代谢的动力学研究中的四个主要发现是:1)apo B合成显著增加; 2)大部分apo B直接进入IDL的生物合成输入; 3)apo B离开IDL的大分解代谢途径; 4)LDL的逐步代谢,通过该代谢产生Sf 20、Sf 10和Sf 4 LDL。
This research concerns the metabolism of apolipoprotein B (apoB) in hypertriglyceridemic subjects with polydisperse or heterogeneous LDL. Five subjects maintained under constant dietary control had blood samples fractionated into very low density lipoprotein (VLDL), Sf 20, Sf 10, and Sf 4 LDL, and plasma free leucine, and in three subjects VLDL was further fractionated by size. Apo B was isolated, and the masses of the plasma apo B pools were measured for these lipoproteins. Following injection of [3H]leucine as a metabolic tracer the specific activity of apo B in these lipoproteins and of plasma leucine were measured over 7 or 14 days. The kinetic data were examined using multicompartmental analysis and interpreted in terms of our previous model of apo B metabolism (1975. Federation Proc. 24: 2263.). Newly synthesized apo B, secreted as large VLDL, is metabolized by a delipidation chain yielding intermediate density lipoprotein (IDL), consisting of small VLDL and Sf 20 LDL, and eventually forms small, Sf4 LDL. LDL is metabolized in a steplike process from Sf 20 to Sf 10 and Sf 4 LDL. A second major biosynthetic input in apo B enters directly into IDL and 1/4 to 2/3 of newly synthesized apo B enters plasma by this route. Total apo B synthesis in these subjects is 5- to 10-fold greater than reported for normals. The rate of transport of VLDL apo B and IDL is slower than normal with a residence time which is increased about twofold; however, the VLDL apo B pool is enlarged 5- to 10-fold, and thus the quantity of apo B entering and leaving this pool per hour is much greater than in the normal. Two major pathways for apo B catabolism occur. Between 1/3 and 2/3 of apo B is metabolized through LDL, disappearing from plasma as Sf 4 LDL. The remainder of apo B disappears from plasma IDL directly. The four major findings in this kinetic study of apo B metabolism in hypertriglyceridemic subjects with polydisperse LDL are: 1) The marking increase in apo B synthesis; 2) the biosynthetic input of much of this apo B directly into IDL; 3) the large catabolic pathway of apo B which leaves IDL, and 4) the stepwise metabolism of LDL by which Sf 20, Sf 10 and Sf 4 LDL are generated.
DOI: 10.1038/sj.bdj.2014.201
发表时间: 2014-03-01
影响因子: 2.6
作者:
Gluskin, A. H.;Peters, C. I.;Peters, O. A.
通讯作者: Peters, O. A.