title: Does genetic variation in the Delta6-desaturase promoter modify the association between alpha-linolenic acid and the prevalence of metabolic syndrome?
abstract: BACKGROUND
  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 Delta(6)-desaturase enzyme converts ALA into EPA and DHA, and genetic variation in the Delta(6)-desaturase gene (FADS2) may affect this conversion.
  
  
  OBJECTIVE
  We hypothesize that high ALA is associated with a lower prevalence of the metabolic syndrome and that genetic variation in FADS2 modifies this association.
  
  
  METHODS
  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.
  
  
  RESULTS
  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).
  
  
  CONCLUSIONS
  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.affiliation: Division of Biology and Medicine, Brown University, Providence, RI 02903, USA.
authors.forename: Hong
authors.initials: H
authors.lastname: Truong
authors.forename: Julia R
authors.initials: JR
authors.lastname: DiBello
authors.forename: Edward
authors.initials: E
authors.lastname: Ruiz-Narvaez
authors.forename: Peter
authors.initials: P
authors.lastname: Kraft
authors.forename: Hannia
authors.initials: H
authors.lastname: Campos
authors.forename: Ana
authors.initials: A
authors.lastname: Baylin
mesh_terms: D000273:Adipose Tissue / Q000201:enzymology / Q000378:metabolism; D000483:Alleles; D003364:Costa Rica / Q000453:epidemiology; D015118:Eicosapentaenoic Acid / Q000378:metabolism; D044943:Fatty Acid Desaturases / Q000235:genetics* / Q000378:metabolism; D017353:Gene Deletion; D005838:Genotype; D006801:Humans; D024821:Metabolic Syndrome / Q000201:enzymology / Q000453:epidemiology / Q000235:genetics* / Q000378:metabolism*; D008875:Middle Aged; D020641:Polymorphism, Single Nucleotide; D015995:Prevalence; D011401:Promoter Regions, Genetic; D012044:Regression Analysis; D017962:alpha-Linolenic Acid / Q000378:metabolism*
chemical_list: D017962:alpha-Linolenic Acid; D015118:Eicosapentaenoic Acid; D044943:Fatty Acid Desaturases; C533241:FADS2 protein, human