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Background  We have previously demonstrated that carrying the apolipoprotein (apo) E epsilon 4 ( E4+ ) genotype disrupts omega-3 fatty acids ( n −  3 PUFA) metabolism. Here we hypothesise that the postprandial clearance of  n −  3 PUFA from the circulation is faster in  E4+  compared to non-carriers ( E4− ). The objective of the study was to investigate the fasted and postprandial fatty acid (FA) profile of triacylglycerol-rich lipoprotein (TRL) fractions: S f  >400 (predominately chylomicron CM), S f  60 − 400 (VLDL 1 ), and S f  20 − 60 (VLDL 2 ) according to  APOE  genotype.    Methods  Postprandial TRL fractions were obtained in 11  E4+  (ϵ3/ϵ4) and 12  E4−  (ϵ3/ϵ3) male from the SATgenϵ study following high saturated fat diet + 3.45 g/d of docosahexaenoic acid (DHA) for 8-wk. Blood samples were taken at fasting and 5-h after consuming a test-meal representative of the dietary intervention. FA were characterized by gas chromatography.    Results  At fasting, there was a 2-fold higher ratio of eicosapentaenoic acid (EPA) to arachidonic acid ( P  = 0.046) as well as a trend towards higher relative% of EPA ( P  = 0.063) in the S f  >400 fraction of  E4+ . Total  n −  3 PUFA in the S f  60 − 400 and S f  20 − 60 fractions were not  APOE  genotype dependant. At 5 h, there was a trend towards a time × genotype interaction ( P  = 0.081) for EPA in the S f  >400 fraction. When sub-groups were form based on the level of EPA at baseline within the S f  >400 fraction, postprandial EPA (%) was significantly reduced only in the high-EPA group. EPA at baseline significantly predicted the postprandial response in EPA only in  E4 + subjects ( R   2   = 0.816).    Conclusion  Despite the DHA supplement contain very low levels of EPA,  E4+  subjects with high EPA at fasting potentially have disrupted postprandial  n −  3 PUFA metabolism after receiving a high-dose of DHA.    Trial registration  Registered at clinicaltrials.gov/show/ NCT01544855 .

Postprandial enrichment of triacylglycerol-rich lipoproteins with omega-3 fatty acids: lack of an interaction with apolipoprotein E genotype?