BACKGROUND: A common G-to-A substitution in the promoter area (-75 base pairs) of the apolipoprotein A-I gene (APOA1) has been described. The A allele was shown to be associated with higher HDL-cholesterol concentrations in some studies but not in others. OBJECTIVE: We examined whether dietary fat modulates the association between this polymorphism and HDL-cholesterol concentrations. DESIGN: We studied a population-based sample of 755 men and 822 women from the Framingham Offspring Study. RESULTS: The frequency of the A allele was 0.165. No significant differences were observed between G/G subjects and carriers of the A allele for any lipid variables. In multivariate linear regression models, HDL-cholesterol concentrations in women were associated with a significant interaction between polyunsaturated fatty acid (PUFA) intake as a continuous variable and APOA1 genotype (P = 0.005). By using 3 categories of PUFA intake, we found a significantly different effect of APOA1 genotype across PUFA categories in women. When PUFA intake was <4% of energy, G/G subjects had approximately 14% higher HDL-cholesterol concentrations than did carriers of the A allele (P < 0.05). Conversely, when PUFA intake was >8%, HDL-cholesterol concentrations in carriers of the A allele were 13% higher than those of G/G subjects (P < 0.05). No significant allelic difference was observed for subjects in the range of PUFA intake of 4-8% of energy. These interactions were not significant in men. CONCLUSIONS: We found a significant gene-diet interaction associated with the APOA1 G-A polymorphism. In women carriers of the A allele, higher PUFA intakes were associated with higher HDL-cholesterol concentrations, whereas the opposite effect was observed in G/G women.
BACKGROUND: A common G-to-A substitution in the promoter area (-75 base pairs) of the apolipoprotein A-I gene (APOA1) has been described. The A allele was shown to be associated with higher HDL-cholesterol concentrations in some studies but not in others. OBJECTIVE: We examined whether dietary fat modulates the association between this polymorphism and HDL-cholesterol concentrations. DESIGN: We studied a population-based sample of 755 men and 822 women from the Framingham Offspring Study. RESULTS: The frequency of the A allele was 0.165. No significant differences were observed between G/G subjects and carriers of the A allele for any lipid variables. In multivariate linear regression models, HDL-cholesterol concentrations in women were associated with a significant interaction between polyunsaturated fatty acid (PUFA) intake as a continuous variable and APOA1 genotype (P = 0.005). By using 3 categories of PUFA intake, we found a significantly different effect of APOA1 genotype across PUFA categories in women. When PUFA intake was <4% of energy, G/G subjects had approximately 14% higher HDL-cholesterol concentrations than did carriers of the A allele (P < 0.05). Conversely, when PUFA intake was >8%, HDL-cholesterol concentrations in carriers of the A allele were 13% higher than those of G/G subjects (P < 0.05). No significant allelic difference was observed for subjects in the range of PUFA intake of 4-8% of energy. These interactions were not significant in men. CONCLUSIONS: We found a significant gene-diet interaction associated with the APOA1 G-A polymorphism. In women carriers of the A allele, higher PUFA intakes were associated with higher HDL-cholesterol concentrations, whereas the opposite effect was observed in G/G women.
Authors: France Gagnon; Gail P Jarvik; Arno G Motulsky; Samir S Deeb; John D Brunzell; Ellen M Wijsman Journal: Hum Genet Date: 2003-08-29 Impact factor: 4.132
Authors: Luigi Barrea; Giuseppe Annunziata; Laura Bordoni; Giovanna Muscogiuri; Annamaria Colao; Silvia Savastano Journal: Int J Obes Suppl Date: 2020-07-20
Authors: Angela M Zivkovic; Michelle M Wiest; Uyenthao Nguyen; Malin L Nording; Steven M Watkins; J Bruce German Journal: Metabolomics Date: 2009 Impact factor: 4.290