title: Postprandial enrichment of triacylglycerol-rich lipoproteins with omega-3 fatty acids: lack of an interaction with apolipoprotein E genotype?
abstract: 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: Sf >400 (predominately chylomicron CM), Sf 60 - 400 (VLDL1), and Sf 20 - 60 (VLDL2) 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 Sf >400 fraction of E4+. Total n - 3 PUFA in the Sf 60 - 400 and Sf 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 Sf >400 fraction. When sub-groups were form based on the level of EPA at baseline within the Sf >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 (R2 = 0.816).
  
  
  CONCLUSIONS
  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.
  
  
  BACKGROUND
  Registered at clinicaltrials.gov/show/NCT01544855.
authors.forename: Valérie
authors.initials: V
authors.lastname: Conway
authors.forename: Marie-Julie
authors.initials: MJ
authors.lastname: Allard
authors.forename: Anne-Marie
authors.initials: AM
authors.lastname: Minihane
authors.forename: Kim G
authors.initials: KG
authors.lastname: Jackson
authors.forename: Julie A
authors.initials: JA
authors.lastname: Lovegrove
authors.affiliation: Centre de recherche sur le vieillissement, Institut Universitaire de Gériatrie de Sherbrooke, Université de Sherbrooke, 1036 Belvédère Sud, Sherbrooke J1H 4C4, Canada. melanie.plourde2@usherbrooke.ca.
authors.forename: Mélanie
authors.initials: M
authors.lastname: Plourde
mesh_terms: D001057:Apolipoproteins E / Q000235:genetics*; D004032:Diet; D004281:Docosahexaenoic Acids / Q000008:administration & dosage* / Q000493:pharmacokinetics; D015118:Eicosapentaenoic Acid / Q000097:blood; D056726:Genetic Association Studies; D006801:Humans; D008079:Lipoproteins, VLDL / Q000097:blood*; D008297:Male; D008875:Middle Aged; D019518:Postprandial Period; D014018:Tissue Distribution; D014280:Triglycerides / Q000097:blood*
chemical_list: D001057:Apolipoproteins E; D008079:Lipoproteins, VLDL; D014280:Triglycerides; D004281:Docosahexaenoic Acids; D015118:Eicosapentaenoic Acid