Birth weight and blood lipid levels in Spanish adolescents: Influence of selected APOE, APOC3 and PPARgamma2 gene polymorphisms. The AVENA Study
Keywords: 
Cardiovascular disease risk
Body-fat composition
Metabolism
Insulin
Issue Date: 
2008
Publisher: 
BioMed Central
ISSN: 
1471-2350
Citation: 
Ruiz JR, Labayen I, Ortega FB, Moreno LA, González-Lamuno D, Marti A, et al. Birth weight and blood lipid levels in Spanish adolescents: Influence of selected APOE, APOC3 and PPARgamma2 gene polymorphisms. The AVENA Study. BMC Med Genet 2008 NOV 10;9:98
Abstract
Background: There is increasing evidence indicating that genes involved in certain metabolic processes of cardiovascular diseases may be of particular influence in people with low body weight at birth. We examined whether the apolipoprotein (APO) E, APOC3 and the peroxisome proliferator-activated receptor-gamma-2 (PPAR gamma 2) polymorphisms influence the association between low birth weight and blood lipid levels in healthy adolescents aged 13-18.5 years. Methods: A cross-sectional study of 502 Spanish adolescents born at term was conducted. Total (TC) and high density lipoprotein cholesterol (HDLc), triglycerides (TG), apolipoprotein (apo) A and B, and lipoprotein(a) [ Lp(a)] were measured. Low density lipoprotein cholesterol (LDLc), TC-HDLc, TC/HDLc and apoB/apoA were calculated. Results: Low birth weight was associated with higher levels of TC, LDLc, apoB, Lp(a), TC-HDLc, TC/HDLc and apoB/apoA in males with the APOE epsilon 3 epsilon 4 genotype, whereas in females, it was associated with lower HDLc and higher TG levels. In males with the APOC3 S1/S2 genotype, low birth weight was associated with lower apoA and higher Lp(a), yet this association was not observed in females. There were no associations between low birth weight and blood lipids in any of the PPAR gamma 2 genotypes. Conclusion: The results indicate that low birth weight has a deleterious influence on lipid profile particularly in adolescents with the APOE epsilon 3/epsilon 4 genotype. These findings suggest that intrauterine environment interact with the genetic background affecting the lipid profile in later life.

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