title: Apolipoprotein E genotype in dyslipidemic patients and response of blood lipids and inflammatory markers to alpha-linolenic Acid.
abstract: The objective of this study was to determine the effect of alpha-linolenic acid (ALA) supplementation on blood lipids and inflammatory markers, in relation to apolipoprotein (apo) E genotype. The diets of 50 dyslipidemic male patients were supplemented with 15 mL of flaxseed oil per day for 12 weeks. Retrospectively, 3 apo E genotype variants were found (epsilon2/epsilon3, n=7; epsilon3/epsilon3, n=33; epsilon3/epsilon4, n=10). No significant differences were found among apo E genotypes in any variables at baseline. ALA supplementation produced a small but significant decrease in high-density lipoprotein cholesterol (from 1.12 to 1.08 mmol/L, 43 to 42 mg/dL; p=0.008) and apo A-I levels (from 1.28 to 1.24 g/L, p=0.036) in the epsilon3/epsilon3 homozygotes. In addition, ALA supplementation resulted in a significant decrease in the serum concentration of serum amyloid A (SAA) (p=0.014), C-reactive protein (CRP) (p=0.013), macrophage colony-stimulating factor (MCSF) (p<0.001), and interleukin (IL)-6 (p=0.028). Serum SAA and MCSF were also significantly decreased in the epsilon3/epsilon4 group (p=0.005 and p=0.017, respectively). In contrast, ALA produced no effects on any of the inflammatory markers in the epsilon2/epsilon3 group. ALA may have beneficial effects on inflammation in dyslipidemic carriers of the apo epsilon3/epsilon3 and epsilon3/epsilon4 genotypes, but not in carriers of the epsilon2 allele.
authors.affiliation: Department of Nutrition and Dietetics, Harokopio University, Athens, Greece.
authors.forename: George K
authors.initials: GK
authors.lastname: Paschos
authors.forename: Nikos
authors.initials: N
authors.lastname: Yiannakouris
authors.forename: Loukianos S
authors.initials: LS
authors.lastname: Rallidis
authors.forename: Ian
authors.initials: I
authors.lastname: Davies
authors.forename: Bruce A
authors.initials: BA
authors.lastname: Griffin
authors.forename: Demosthenes B
authors.initials: DB
authors.lastname: Panagiotakos
authors.forename: Fotini N
authors.initials: FN
authors.lastname: Skopouli
authors.forename: Vasilios
authors.initials: V
authors.lastname: Votteas
authors.forename: Antonis
authors.initials: A
authors.lastname: Zampelas
mesh_terms: D000328:Adult; D000368:Aged; D053329:Apolipoprotein E2; D053318:Apolipoprotein E3; D053327:Apolipoprotein E4; D001057:Apolipoproteins E / Q000235:genetics*; D008076:Cholesterol, HDL / Q000097:blood; D003324:Coronary Artery Disease / Q000097:blood / Q000235:genetics / Q000517:prevention & control; D019587:Dietary Supplements; D014644:Genetic Variation; D005838:Genotype; D006115:Greece; D006720:Homozygote; D006801:Humans; D006949:Hyperlipidemias / Q000097:blood / Q000178:diet therapy* / Q000235:genetics; D018836:Inflammation Mediators / Q000097:blood*; D008043:Linseed Oil / Q000008:administration & dosage*; D008055:Lipids / Q000097:blood*; D008297:Male; D008875:Middle Aged; D015596:Nutrition Assessment; D011110:Polymorphism, Genetic; D012307:Risk Factors; D000685:Serum Amyloid A Protein / Q000378:metabolism; D016896:Treatment Outcome; D017962:alpha-Linolenic Acid / Q000008:administration & dosage*
chemical_list: D053329:Apolipoprotein E2; D053318:Apolipoprotein E3; D053327:Apolipoprotein E4; D001057:Apolipoproteins E; D008076:Cholesterol, HDL; D018836:Inflammation Mediators; D008055:Lipids; D000685:Serum Amyloid A Protein; D017962:alpha-Linolenic Acid; D008043:Linseed Oil