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Contribution of apolipoprotein E genotype and docosahexaenoic acid to the LDL-cholesterol response to fish oil.
Atherosclerosis. 2010 Mar; 209(1):104-10.A

Abstract

OBJECTIVES

To investigate the impact of apolipoprotein E (apoE) genotype on the response of the plasma lipoprotein profile to eicosapentaenoic acid (EPA) versus docosahexaenoic acid (DHA) intervention in humans.

METHODS AND RESULTS

38 healthy normolipidaemic males, prospectively recruited on the basis of apoE genotype (n=20 E3/E3 and n=18 E3/E4), completed a double-blind placebo-controlled cross-over trial, consisting of 3 x 4 week intervention arms of either control oil, EPA-rich oil (ERO, 3.3g EPA/day) or DHA-rich oil (DRO, 3.7g DHA/day) in random order, separated by 10 week wash-out periods. A significant genotype-independent 28% and 19% reduction in plasma triglycerides in response to ERO and DRO was observed. For total cholesterol (TC), no significant treatment effects were evident; however a significant genotype by treatment interaction emerged (P=0.045), with a differential response to ERO and DRO in E4 carriers. Although the genotype x treatment interaction for LDL-cholesterol (P=0.089) did not reach significance, within DRO treatment analysis indicated a 10% increase in LDL (P=0.029) in E4 carriers with a non-significant 4% reduction in E3/E3 individuals. A genotype-independent increase in LDL mass was observed following DRO intervention (P=0.018). Competitive uptake studies in HepG2 cells using plasma very low density lipoproteins (VLDL) from the human trial, indicated that following DRO treatment, VLDL(2) fractions obtained from E3/E4 individuals resulted in a significant 32% (P=0.002) reduction in LDL uptake relative to the control.

CONCLUSIONS

High dose DHA supplementation is associated with increases in total cholesterol in E4 carriers, which appears to be due to an increase in LDL-C and may in part negate the cardioprotective action of DHA in this population subgroup.

Authors+Show Affiliations

Hugh Sinclair Unit of Nutrition, School of Chemistry, Food Biosciences and Pharmacy, University of Reading, Reading, UK.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Controlled Clinical Trial
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

19748619

Citation

Olano-Martin, Estibaliz, et al. "Contribution of Apolipoprotein E Genotype and Docosahexaenoic Acid to the LDL-cholesterol Response to Fish Oil." Atherosclerosis, vol. 209, no. 1, 2010, pp. 104-10.
Olano-Martin E, Anil E, Caslake MJ, et al. Contribution of apolipoprotein E genotype and docosahexaenoic acid to the LDL-cholesterol response to fish oil. Atherosclerosis. 2010;209(1):104-10.
Olano-Martin, E., Anil, E., Caslake, M. J., Packard, C. J., Bedford, D., Stewart, G., Peiris, D., Williams, C. M., & Minihane, A. M. (2010). Contribution of apolipoprotein E genotype and docosahexaenoic acid to the LDL-cholesterol response to fish oil. Atherosclerosis, 209(1), 104-10. https://doi.org/10.1016/j.atherosclerosis.2009.08.024
Olano-Martin E, et al. Contribution of Apolipoprotein E Genotype and Docosahexaenoic Acid to the LDL-cholesterol Response to Fish Oil. Atherosclerosis. 2010;209(1):104-10. PubMed PMID: 19748619.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Contribution of apolipoprotein E genotype and docosahexaenoic acid to the LDL-cholesterol response to fish oil. AU - Olano-Martin,Estibaliz, AU - Anil,Eliz, AU - Caslake,Muriel J, AU - Packard,Chris J, AU - Bedford,Dorothy, AU - Stewart,Grace, AU - Peiris,Dammika, AU - Williams,Christine M, AU - Minihane,Anne M, Y1 - 2009/08/21/ PY - 2009/01/09/received PY - 2009/08/09/revised PY - 2009/08/14/accepted PY - 2009/9/15/entrez PY - 2009/9/15/pubmed PY - 2010/6/5/medline SP - 104 EP - 10 JF - Atherosclerosis JO - Atherosclerosis VL - 209 IS - 1 N2 - OBJECTIVES: To investigate the impact of apolipoprotein E (apoE) genotype on the response of the plasma lipoprotein profile to eicosapentaenoic acid (EPA) versus docosahexaenoic acid (DHA) intervention in humans. METHODS AND RESULTS: 38 healthy normolipidaemic males, prospectively recruited on the basis of apoE genotype (n=20 E3/E3 and n=18 E3/E4), completed a double-blind placebo-controlled cross-over trial, consisting of 3 x 4 week intervention arms of either control oil, EPA-rich oil (ERO, 3.3g EPA/day) or DHA-rich oil (DRO, 3.7g DHA/day) in random order, separated by 10 week wash-out periods. A significant genotype-independent 28% and 19% reduction in plasma triglycerides in response to ERO and DRO was observed. For total cholesterol (TC), no significant treatment effects were evident; however a significant genotype by treatment interaction emerged (P=0.045), with a differential response to ERO and DRO in E4 carriers. Although the genotype x treatment interaction for LDL-cholesterol (P=0.089) did not reach significance, within DRO treatment analysis indicated a 10% increase in LDL (P=0.029) in E4 carriers with a non-significant 4% reduction in E3/E3 individuals. A genotype-independent increase in LDL mass was observed following DRO intervention (P=0.018). Competitive uptake studies in HepG2 cells using plasma very low density lipoproteins (VLDL) from the human trial, indicated that following DRO treatment, VLDL(2) fractions obtained from E3/E4 individuals resulted in a significant 32% (P=0.002) reduction in LDL uptake relative to the control. CONCLUSIONS: High dose DHA supplementation is associated with increases in total cholesterol in E4 carriers, which appears to be due to an increase in LDL-C and may in part negate the cardioprotective action of DHA in this population subgroup. SN - 1879-1484 UR - https://www.unboundmedicine.com/medline/citation/19748619/Contribution_of_apolipoprotein_E_genotype_and_docosahexaenoic_acid_to_the_LDL_cholesterol_response_to_fish_oil_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0021-9150(09)00686-8 DB - PRIME DP - Unbound Medicine ER -