title: 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.
abstract: 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.
authors.affiliation: Department of Epidemiology, Tulane Center for Cardiovascular Health, Tulane School of Public Health & Tropical Medicine, 1440 Canal Street, Suite 2140, New Orleans, LA 70112, USA.
authors.forename: W
authors.initials: W
authors.lastname: Chen
authors.forename: S R
authors.initials: SR
authors.lastname: Srinivasan
authors.forename: A
authors.initials: A
authors.lastname: Elkasabany
authors.forename: D L
authors.initials: DL
authors.lastname: Ellsworth
authors.forename: E
authors.initials: E
authors.lastname: Boerwinkle
authors.forename: G S
authors.initials: GS
authors.lastname: Berenson
mesh_terms: D000293:Adolescent; D000328:Adult; D008076:Cholesterol, HDL / Q000032:analysis*; D003324:Coronary Artery Disease / Q000175:diagnosis / Q000453:epidemiology / Q000235:genetics*; D003430:Cross-Sectional Studies; D003625:Data Collection; D005260:Female; D020022:Genetic Predisposition to Disease; D014644:Genetic Variation; D006801:Humans; D008071:Lipoprotein Lipase / Q000235:genetics*; D008297:Male; D011336:Probability; D011401:Promoter Regions, Genetic; D012680:Sensitivity and Specificity; D012694:Serine / Q000235:genetics*; D014280:Triglycerides / Q000032:analysis*
chemical_list: D008076:Cholesterol, HDL; D014280:Triglycerides; D012694:Serine; D008071:Lipoprotein Lipase