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ARS Home » Northeast Area » Boston, Massachusetts » Research » Publications at this Location » Publication #284783
Title: Genetic variation in fatty acid elongases is not associated with intermediate cardiovascular phenotypes or myocardial infarction

Author
item ASLIBEKYAN, STELLA - Brown University
item JENSEN, MAJKEN - Harvard School Of Public Health
item CAMPOS, HANNIA - Harvard School Of Public Health
item LINKLETTER, CRYSTAL - Brown University
item LOUCKS, ERIC - Brown University
item ORDOVAS, JOSE - Jean Mayer Human Nutrition Research Center On Aging At Tufts University
item DEKA, RANJAN - University Of Cincinnati
item RIMM, ERIC - Harvard School Of Public Health
item BAYLIN, ANA - University Of Michigan

Submitted to: European Journal of Clinical Nutrition
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 1/4/2012
Publication Date: 3/1/2012
Citation: Aslibekyan, S., Jensen, M.K., Campos, H., Linkletter, C.D., Loucks, E.B., Ordovas, J.M., Deka, R., Rimm, E.B., Baylin, A. 2012. Genetic variation in fatty acid elongases is not associated with intermediate cardiovascular phenotypes or myocardial infarction. European Journal of Clinical Nutrition. 66(3):353-359.

Interpretive Summary: 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 (rs174556, rs3834458, rs174570, rs2524299, rs174589, rs174627) were associated with cardiovascular risk factors, and non-fatal heart attack (myocardial infarction -MI) in a case-control study of Costa Rican adults (1650 cases and 1650 controls). Moreover, analyses involving cardiovascular risk factors and MI were also conducted in two replication cohorts, The Nurses' Health Study (n = 1200) and The Health Professionals Follow-Up Study (n = 1295). 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 low-density lipoprotein (LDL) cholesterol. 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. However, the observed associations were not replicated in independent populations. Therefore, genetic variants in elongases are not consistently associated with adipose tissue fatty acids, serum lipids, biomarkers of systemic inflammation, or the risk of MI.

Technical Abstract: 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. 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). 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 less than 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. Common genetic variants in elongases are not associated with adipose tissue fatty acids, serum lipids, biomarkers of systemic inflammation, or the risk of MI.