title: Genetic variation in fatty acid elongases is not associated with intermediate cardiovascular phenotypes or myocardial infarction.
abstract: OBJECTIVE
  Elongases 2, 4 and 5, encoded by genes ELOVL2, ELOVL4 and ELOVL5, have a key role in the biosynthesis of very long chain polyunsaturated fatty acids (PUFAs). To date, few studies have investigated the associations between elongase polymorphisms and cardiovascular health. We investigated whether ELOVL polymorphisms are associated with adipose tissue fatty acids, serum lipids, inflammation and ultimately with nonfatal myocardial infarction (MI) in a Costa Rican population.
  
  
  METHODS
  MI cases (n=1650) were matched to population-based controls (n=1650) on age, sex and area of residence. Generalized linear and multiple conditional logistic regression models were used to assess the associations between seven common ELOVL polymorphisms and cardiometabolic outcomes. Analyses were replicated in The Nurses' Health Study (n=1200) and The Health Professionals Follow-Up Study (n=1295).
  
  
  RESULTS
  Variation in ELOVL2, ELOVL4 and ELOVL5 was not associated with adipose tissue fatty acids, intermediate cardiovascular risk factors or MI. In the Costa Rica study, the number of the minor allele copies at rs2294867, located in the ELOVL5 gene, was associated with an increase in total and LDL cholesterol (adjusted P-values=0.001 and <0.0001 respectively). Additionally, the number of the minor allele copies at rs761179, also located in the ELOVL5 gene, was significantly associated with an increase in total cholesterol (adjusted P-value=0.04). However, the observed associations were not replicated in independent populations.
  
  
  CONCLUSIONS
  Common genetic variants in elongases are not associated with adipose tissue fatty acids, serum lipids, biomarkers of systemic inflammation, or the risk of MI.
authors.affiliation: Department of Community Health, Brown University, Providence, RI, USA.
authors.forename: S
authors.initials: S
authors.lastname: Aslibekyan
authors.forename: M K
authors.initials: MK
authors.lastname: Jensen
authors.forename: H
authors.initials: H
authors.lastname: Campos
authors.forename: C D
authors.initials: CD
authors.lastname: Linkletter
authors.forename: E B
authors.initials: EB
authors.lastname: Loucks
authors.forename: J M
authors.initials: JM
authors.lastname: Ordovas
authors.forename: R
authors.initials: R
authors.lastname: Deka
authors.forename: E B
authors.initials: EB
authors.lastname: Rimm
authors.forename: A
authors.initials: A
authors.lastname: Baylin
mesh_terms: D000123:Acetyltransferases / Q000235:genetics*; D000273:Adipose Tissue / Q000378:metabolism; D000368:Aged; D000483:Alleles; D002318:Cardiovascular Diseases / Q000235:genetics*; D016022:Case-Control Studies; D002784:Cholesterol / Q000097:blood / Q000235:genetics*; D008078:Cholesterol, LDL / Q000097:blood / Q000235:genetics; D003364:Costa Rica; D000081031:Fatty Acid Elongases; D005231:Fatty Acids, Unsaturated / Q000096:biosynthesis / Q000235:genetics*; D005260:Female; D005838:Genotype; D006801:Humans; D007249:Inflammation / Q000235:genetics*; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000235:genetics*; D010641:Phenotype; D011110:Polymorphism, Genetic; D012307:Risk Factors
chemical_list: D008078:Cholesterol, LDL; C000630967:ELOVL2 protein, human; C000630954:ELOVL5 protein, human; D005231:Fatty Acids, Unsaturated; D002784:Cholesterol; D000123:Acetyltransferases; D000081031:Fatty Acid Elongases