title: APOE genotype influences triglyceride and C-reactive protein responses to altered dietary fat intake in UK adults.
abstract: BACKGROUND
  The response of plasma lipids to dietary fat manipulation is highly heterogeneous, with some indications that APOE genotype may be important.
  
  
  OBJECTIVE
  The objective was to use a prospective recruitment approach to determine the effect of dietary fat quantity and composition on both lipid and nonlipid cardiovascular disease biomarkers according to APOE genotype.
  
  
  METHODS
  Participants had a mean (±SD) age of 51 ± 9 y and a BMI (in kg/m²) of 26.0 ± 3.8 (n = 44 E3/E3, n = 44 E3/E4) and followed a sequential dietary intervention (the SATgenε study) in which they were assigned to a low-fat diet, a high-fat high-SFA (HSF) diet, and the HSF diet with 3.45 g DHA/d (HSF-DHA), each for 8 wk. Fasting blood samples were collected at the end of each intervention arm.
  
  
  RESULTS
  An overall diet effect was evident for all cholesterol fractions (P < 0.01), with no significant genotype × diet interactions observed. A genotype × diet interaction (P = 0.033) was evident for plasma triglycerides, with 17% and 30% decreases in APOE3/E3 and APOE3/E4 individuals after the HSF-DHA diet relative to the low-fat diet. A significant genotype × diet interaction (P = 0.009) was also observed for C-reactive protein (CRP), with only significant increases in concentrations after the HSF and HSF-DHA diets relative to the low-fat diet in the APOE3/E4 group (P < 0.015).
  
  
  CONCLUSIONS
  Relative to the wild-type APOE3/E3 group, our results indicate a greater sensitivity of fasting triglycerides and CRP to dietary fat manipulation in those with an APOE3/E4 genotype (25% population), with no effect of this allelic profile on cholesterol concentrations.
authors.affiliation: Hugh Sinclair Unit of Human Nutrition and Institute for Cardiovascular and Metabolic Research, Department of Food and Nutritional Sciences, University of Reading, Reading, United Kingdom.
authors.forename: Andrew L
authors.initials: AL
authors.lastname: Carvalho-Wells
authors.forename: Kim G
authors.initials: KG
authors.lastname: Jackson
authors.forename: Stacey
authors.initials: S
authors.lastname: Lockyer
authors.forename: Julie A
authors.initials: JA
authors.lastname: Lovegrove
authors.forename: Anne M
authors.initials: AM
authors.lastname: Minihane
mesh_terms: D000328:Adult; D000368:Aged; D053318:Apolipoprotein E3 / Q000097:blood / Q000235:genetics* / Q000378:metabolism; D053327:Apolipoprotein E4 / Q000097:blood / Q000235:genetics* / Q000378:metabolism; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000032:analysis*; D002318:Cardiovascular Diseases / Q000453:epidemiology / Q000276:immunology / Q000517:prevention & control; D008078:Cholesterol, LDL / Q000097:blood; D018752:Diet, Fat-Restricted; D059305:Diet, High-Fat / Q000009:adverse effects; D004281:Docosahexaenoic Acids / Q000627:therapeutic use; D005260:Female; D056726:Genetic Association Studies; D006801:Humans; D006937:Hypercholesterolemia / Q000178:diet therapy / Q000209:etiology / Q000235:genetics / Q000378:metabolism; D015228:Hypertriglyceridemia / Q000178:diet therapy* / Q000209:etiology / Q000235:genetics / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D020641:Polymorphism, Single Nucleotide; D012307:Risk Factors; D014280:Triglycerides / Q000097:blood*; D006113:United Kingdom / Q000453:epidemiology
chemical_list: D053318:Apolipoprotein E3; D053327:Apolipoprotein E4; D015415:Biomarkers; D008078:Cholesterol, LDL; D014280:Triglycerides; D004281:Docosahexaenoic Acids; D002097:C-Reactive Protein