APOE genotype influences triglyceride and C-reactive protein responses to altered dietary fat intake in UK adults

Am J Clin Nutr. 2012 Dec;96(6):1447-53. doi: 10.3945/ajcn.112.043240. Epub 2012 Nov 7.

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.

Design: 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.

Trial registration: ClinicalTrials.gov NCT01384032.

Publication types

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

MeSH terms

  • Adult
  • Aged
  • Apolipoprotein E3 / blood
  • Apolipoprotein E3 / genetics*
  • Apolipoprotein E3 / metabolism
  • Apolipoprotein E4 / blood
  • Apolipoprotein E4 / genetics*
  • Apolipoprotein E4 / metabolism
  • Biomarkers / blood
  • C-Reactive Protein / analysis*
  • Cardiovascular Diseases / epidemiology
  • Cardiovascular Diseases / immunology
  • Cardiovascular Diseases / prevention & control
  • Cholesterol, LDL / blood
  • Diet, Fat-Restricted*
  • Diet, High-Fat / adverse effects
  • Docosahexaenoic Acids / therapeutic use
  • Female
  • Genetic Association Studies
  • Humans
  • Hypercholesterolemia / diet therapy
  • Hypercholesterolemia / etiology
  • Hypercholesterolemia / genetics
  • Hypercholesterolemia / metabolism
  • Hypertriglyceridemia / diet therapy*
  • Hypertriglyceridemia / etiology
  • Hypertriglyceridemia / genetics
  • Hypertriglyceridemia / metabolism
  • Male
  • Middle Aged
  • Polymorphism, Single Nucleotide*
  • Risk Factors
  • Triglycerides / blood*
  • United Kingdom / epidemiology

Substances

  • Apolipoprotein E3
  • Apolipoprotein E4
  • Biomarkers
  • Cholesterol, LDL
  • Triglycerides
  • Docosahexaenoic Acids
  • C-Reactive Protein

Associated data

  • ClinicalTrials.gov/NCT01384032