Influence of lipoprotein lipase serine 447 stop polymorphism on tracking of triglycerides and HDL cholesterol from childhood to adulthood and familial risk of coronary artery disease: the Bogalusa Heart Study

被引:33
作者
Chen, W
Srinivasan, SR
Elkasabany, A
Ellsworth, DL
Boerwinkle, E
Berenson, GS
机构
[1] Tulane Sch Publ Hlth & Trop Med, Ctr Cardiovasc Hlth, Dept Epidemiol, New Orleans, LA 70112 USA
[2] NHLBI, Div Epidemiol & Clin Applicat, NIH, Bethesda, MD 20892 USA
[3] Univ Texas, Houston Hlth Sci Ctr, Inst Mol Med, Ctr Human Genet, Houston, TX USA
关键词
lipoprotein lipase S447X polymorphism; lipoproteins; tracking; coronary disease;
D O I
10.1016/S0021-9150(01)00508-1
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The effects of the lipoprotein lipase (LPL) Serine 447 Stop (S447X) polymorphism on high-density lipoprotein cholesterol (HDLC) and triglycerides (TG) have been demonstrated. However, little is known about its effect on the tracking of HDLC and TG over time and familial risk of coronary artery disease (CAD). This aspect was examined in black and white individuals (n = 829) aged 5-18 year at baseline, followed on average 18.8 yr. The frequency of the X447 allele was lower in Blacks than Whites (0.043 vs 0.087, P = 0.002). Carriers vs noncarriers of the X447 allele had lower TG (99.3 vs 122.1 mg/dl, P < 0.01) and higher HDLC (51.1 vs 49.7 mg/dl, P < 0.05) in adulthood, but not in childhood. The trends in genotype-specific means of childhood and adulthood levels of HDLC and TG in sex or race subgroups were similar to those in the total sample. With respect to tracking over time, of those in the bottom quartile of HDLC in childhood, 46.1% of the noncarriers vs 23.1% of the carriers remained in this lowest quartile into adulthood (P = 0.03); corresponding values for the top quartile of HDLC were 37.5% for the noncarriers vs 57.1% for the carriers (P = 0.03). Although TG tended to track better among the carriers in the bottom quartile and among the noncarriers in the top quartile, this trend was not significant. Carriers showed lower prevalence of parental history of CAD than noncarriers (6.9% vs 14.1%, P = 0.02) independently of lipoprotein variables, adiposity, blood pressure, age, sex and race. Thus, the X447 allele of the LPL gene is associated with an increase in HDLC and a decrease in TG in adults, tracking of HDLC since childhood, and a lower family history of CAD. (C) 2001 Elsevier Science Ireland Ltd. All rights reserved.
引用
收藏
页码:367 / 373
页数:7
相关论文
共 39 条
  • [1] AMA PFM, 1986, INT J OBESITY, V10, P503
  • [2] [Anonymous], 1995, AM J MED SCI, V310, pS1
  • [3] Berenson GS, 1980, CARDIOVASCULAR RISK
  • [4] BERG K, 1989, ARTERIOSCLEROSIS S, V9, P50
  • [5] Black-white differences in postprandial triglyceride response and postheparin lipoprotein lipase and hepatic triglyceride lipase among young men
    Friday, KE
    Srinivasan, SR
    Elkasabany, A
    Dong, CP
    Wattigney, WA
    Dalferes, E
    Berenson, GS
    [J]. METABOLISM-CLINICAL AND EXPERIMENTAL, 1999, 48 (06): : 749 - 754
  • [6] A common truncation variant of lipoprotein lipase (Ser447X) confers protection against coronary heart disease:: the Framingham Offspring Study
    Gagné, SE
    Larson, MG
    Pimstone, SN
    Schaefer, EJ
    Kastelein, JJP
    Wilson, PWF
    Ordovas, JM
    Hayden, MR
    [J]. CLINICAL GENETICS, 1999, 55 (06) : 450 - 454
  • [7] HIGH-DENSITY LIPOPROTEIN CHOLESTEROL AND CARDIOVASCULAR-DISEASE - 4 PROSPECTIVE AMERICAN-STUDIES
    GORDON, DJ
    PROBSTFIELD, JL
    GARRISON, RJ
    NEATON, JD
    CASTELLI, WP
    KNOKE, JD
    JACOBS, DR
    BANGDIWALA, S
    TYROLER, HA
    [J]. CIRCULATION, 1989, 79 (01) : 8 - 15
  • [8] Genetic variant showing a positive interaction with beta-blocking agents with a beneficial influence on lipoprotein lipase activity, HDL cholesterol, and triglyceride levels in coronary artery disease patients - The Ser(447)-Stop substitution in the lipoprotein lipase gene
    Groenemeijer, BE
    Hallman, MD
    Reymer, PWA
    Gagne, E
    Kuivenhoven, JA
    Bruin, T
    Jansen, H
    Lie, KI
    Bruschke, AVG
    Boerwinkle, E
    Hayden, MR
    Kastelein, JJP
    [J]. CIRCULATION, 1997, 95 (12) : 2628 - 2635
  • [9] Hall S, 2000, GENET EPIDEMIOL, V18, P203, DOI 10.1002/(SICI)1098-2272(200003)18:3<203::AID-GEPI2>3.0.CO
  • [10] 2-I