Does genetic variation in the Δ6 -desaturase promoter modify the
Does genetic variation in the Δ6 -desaturase promoter modify the
Year: 2009
Authors: Truong, H. DiBello, J.R. Ruiz-Narvaez, E. Kraft, P. Campos, H. Baylin, A.
Publication Name: Am. J. Clin. Nutr.
Publication Details: Volume 89; Pages 920 – 925.
Abstract:
Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are associated with protection against components of the metabolic syndrome, but the role of alpha-linolenic acid (ALA), the metabolic precursor of EPA and DHA, has not been studied. The D6-desaturase enzyme converts ALA into EPA and DHA, and genetic variation in the D6-desaturase gene (FADS2) may affect this conversion. We hypothesize that high ALA is associated with a lower prevalence of the metabolic syndrome and that genetic variation in FADS2 modifies this association. We studied 1815 Costa Rican adults. Adipose tissue ALA was used as a biomarker of intake, and metabolic syndrome was identified with the definition from the National Cholesterol Education Program, Adult Treatment Panel III. Prevalence ratios (PRs) and 95% CIs were estimated from binomial regression models, and the likelihood ratio was used to test for effect modification. High concentrations of adipose tissue ALA were associated with lower PRs of the metabolic syndrome compared with low ALA (0.81; 95% CI: 0.66, 1.00, for the comparison between the highest and the lowest quintiles; P for trend 0.02). Higher concentrations of adipose tissue ALA were associated with a lower PR among homozygote (0.67; 95% CI: 0.53, 0.86) and heterozygote (0.84; 95% CI: 0.72, 0.99) carriers of the FADS2 T allele, but not among homozygote carriers of the deletion variant allele (0.99; 95% CI: 0.78, 1.27; P for interaction: 0.08). Elevated ALA concentrations in adipose tissue are associated with lower prevalence of the metabolic syndrome. A lack of association among homozygote carriers of the FADS2 deletion allele suggests that this association may be due in part to the conversion of ALA into EPA. (Authors abstract)
The collection of metabolic risk factors that define the metabolic syndrome include obesity, high blood pressure and plasma triglyceride concentrations, low HDL cholesterol, and impaired fasting glucose among others. Alpha-Linolenic acid (ALA; 18:3n3) may be a sustainable alternative to achieve a higher intake of n3 fatty acids. A high intake of vegetable oils rich in ALA elevates plasma lipid fractions and neutrophil phospholipids concentrations of EPA to an amount comparable to that of a diet supplemented with fish oil when the background intakes of linoleic acid, EPA, and DHA are low. The presence of a variant T to deletion (T del) in the promoter of the D6 desaturase gene (FADS2) leads to reduced EPA concentrations in plasma and adipose tissue, suggesting that this variant decreases enzyme activity and therefore conversion from ALA. The purpose of this study was to 1) examine whether increased ALA is associated with a lower prevalence of the metabolic syndrome and 2) test whether this association is modified by the FADS2 T del variant. Subjects with higher concentrations of adipose tissue ALA had lower PRs for metabolic syndrome than did subjects with low concentrations of adipose tissue ALA. Furthermore, a lack of association among homozygote carriers of the FADS2 deletion allele suggests that this association may be due in part to the conversion of ALA into EPA. Evidence about the direct effect of ALA on the metabolic syndrome is scarce The association between ALA and metabolic syndrome seen in this study may be due to the many protective properties of the metabolites of ALA, EPA and DHA. A higher prevalence of metabolic syndrome among those homozygous for this variant suggests that the potential protective properties of ALA may be due to its metabolism into long-chain n3 fatty acids. In conclusion, the authors found an association between high concentrations of adipose ALA and a decreased prevalence of the metabolic syndrome within a Costa Rican population with low fish intake. Furthermore, a novel relation between the FADS2 variant, ALA, and metabolic syndrome was found, suggesting that genetic variation may play an important role along with diet in the development of the metabolic syndrome in this population. Future studies will be of special importance in those populations in which the intake of ALA and long-chain n3 fatty acids (EPA and DHA) from fish is low. (Editors Comments)
The collection of metabolic risk factors that define the metabolic syndrome include obesity, high blood pressure and plasma triglyceride concentrations, low HDL cholesterol, and impaired fasting glucose among others. Alpha-Linolenic acid (ALA; 18:3n3) may be a sustainable alternative to achieve a higher intake of n3 fatty acids. A high intake of vegetable oils rich in ALA elevates plasma lipid fractions and neutrophil phospholipids concentrations of EPA to an amount comparable to that of a diet supplemented with fish oil when the background intakes of linoleic acid, EPA, and DHA are low. The presence of a variant T to deletion (T del) in the promoter of the D6 desaturase gene (FADS2) leads to reduced EPA concentrations in plasma and adipose tissue, suggesting that this variant decreases enzyme activity and therefore conversion from ALA. The purpose of this study was to 1) examine whether increased ALA is associated with a lower prevalence of the metabolic syndrome and 2) test whether this association is modified by the FADS2 T del variant. Subjects with higher concentrations of adipose tissue ALA had lower PRs for metabolic syndrome than did subjects with low concentrations of adipose tissue ALA. Furthermore, a lack of association among homozygote carriers of the FADS2 deletion allele suggests that this association may be due in part to the conversion of ALA into EPA. Evidence about the direct effect of ALA on the metabolic syndrome is scarce The association between ALA and metabolic syndrome seen in this study may be due to the many protective properties of the metabolites of ALA, EPA and DHA. A higher prevalence of metabolic syndrome among those homozygous for this variant suggests that the potential protective properties of ALA may be due to its metabolism into long-chain n3 fatty acids. In conclusion, the authors found an association between high concentrations of adipose ALA and a decreased prevalence of the metabolic syndrome within a Costa Rican population with low fish intake. Furthermore, a novel relation between the FADS2 variant, ALA, and metabolic syndrome was found, suggesting that genetic variation may play an important role along with diet in the development of the metabolic syndrome in this population. Future studies will be of special importance in those populations in which the intake of ALA and long-chain n3 fatty acids (EPA and DHA) from fish is low. (Editors Comments)
