ApoE phenotype influences plasma ASP in hyperapoB subjects

被引:2
作者
Cianflone, K
Phélis, S
Davignon, J
Gilfix, BM
机构
[1] McGill Univ, Royal Victoria Hosp, Ctr Hlth, Mike Rosenbloom Lab Cardiovasc Res, Montreal, PQ H3A 1A1, Canada
[2] Royal Victoria Hosp, Montreal, PQ H3A 1A1, Canada
[3] Inst Rech Clin Montreal, Montreal, PQ H2W 1R7, Canada
基金
加拿大健康研究院;
关键词
C3a desArg; non-esterified fatty acids; triglyceride; cholesterol;
D O I
10.1016/S0021-9150(03)00289-2
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Acylation stimulating protein (ASP) is increased in cardiovascular patients who often present with dyslipidemias. The aim of the present study was to examine the influence of apolipoprotein E (apoE) phenotype and lipids on ASP. Plasma ASP, lipids and apoE phenotype were measured in 407 subjects and separated according to the 75th percentile of apolipoprotein B (apoB) into a HyperapoB (HB) group (apoB = 152 +/- 34 mg/dl, 117 men, 80 women) and a normal apoB (NB) group (apoB = 88 +/- 19 mg/dl, 126 men, 84 women). Triglyceride (TG), cholesterol and LDL cholesterol were significantly increased in HB versus NB but there was no difference in age or body mass index (BMI). HB had increased ASP (42%>75th percentile, median = 48.4 nM, P < 0.001) versus NB (36.5 nM). There was no difference in ASP in NB with any apoE3 variant (E3/3 = 41 nM, n = 98; E3/4 = 46 nM, n = 55; E3/2 = 50 nM, n = 41), but ASP was increased in E2/2 (126 nM, n = 9), and E4/4 (186 nM, n = 5, P < 0.001 ANOVA). In HB, ASP was increased in three apoE phenotypes: E2/4 (209 nM, n = 6), E2/2 (135 nM, n = 6) and E4/4 (189 nM, n = 26), P < 0.00 1 ANOVA relative to the other apoE phenotypes (E3/3 = 50 nM, n = 102; E3/4 = 41 nM, n = 40; E3/2 = 87 nM, n = 17) with a wide range of values. By stepwise regression analysis, the best model that predicted ASP was: [plasma non-esterified fatty acid (NEFA) + TG + cholesterol], where r = 0,407, P = 0.001. These data suggest that apoE phenotype may potentially influence ASP, although primarily in rare apoE phenotypes. (C)2003 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:285 / 291
页数:7
相关论文
共 60 条
[1]   THE ADIPSIN ACYLATION STIMULATING PROTEIN SYSTEM AND REGULATION OF INTRACELLULAR TRIGLYCERIDE SYNTHESIS [J].
BALDO, A ;
SNIDERMAN, AD ;
STLUCE, S ;
AVRAMOGLU, RK ;
MASLOWSKA, M ;
HOANG, B ;
MONGE, JC ;
BELL, A ;
MULAY, S ;
CIANFLONE, K .
JOURNAL OF CLINICAL INVESTIGATION, 1993, 92 (03) :1543-1547
[2]   Prolonged postprandial responses of lipids and apolipoproteins in triglyceride-rich lipoproteins of individuals expressing an apolipoprotein epsilon 4 allele [J].
Bergeron, N ;
Havel, RJ .
JOURNAL OF CLINICAL INVESTIGATION, 1996, 97 (01) :65-72
[3]  
BOERWINKLE E, 1994, AM J HUM GENET, V54, P341
[4]   MOLECULAR-BASIS OF POLYMORPHISMS OF HUMAN-COMPLEMENT COMPONENT-C3 [J].
BOTTO, M ;
FONG, KY ;
SO, AK ;
KOCH, C ;
WALPORT, MJ .
JOURNAL OF EXPERIMENTAL MEDICINE, 1990, 172 (04) :1011-1017
[5]  
BOUTHILLIER D, 1983, J LIPID RES, V24, P1060
[6]  
Brown R., 1999, HOMOL HOMOTOPY APPL, V1, P1, DOI [DOI 10.4310/HHA.1999.V1.N1.A1, 10.4310/HHA.1999.v1.n1.a1, 10.4310/HHA.1999.v1.n1.a1.165,171,173,221]
[7]  
CIANFLONE K, 1995, INT J OBESITY, V19, P604
[8]  
Cianflone K, 1997, ARTERIOSCL THROM VAS, V17, P1239
[9]   Critical review of acylation-stimulating protein physiology in humans and rodents [J].
Cianflone, K ;
Xia, ZN ;
Chen, LY .
BIOCHIMICA ET BIOPHYSICA ACTA-BIOMEMBRANES, 2003, 1609 (02) :127-143
[10]  
CIANFLONE K, 1988, CLIN INVEST MED, V11, P99