title: Serum lipid and blood pressure responses to quercetin vary in overweight patients by apolipoprotein E genotype.
abstract: Our objective was to examine the effect of a quercetin supplementation on blood pressure, lipid metabolism, markers of oxidative stress, inflammation, and body composition in an at-risk population of 93 overweight-obese volunteers aged 25-65 y with metabolic syndrome traits in relation to apolipoprotein (apo) E genotype. Participants were randomized to receive 150 mg/d quercetin in a double-blinded, placebo-controlled, crossover trial with 6-wk treatment periods separated by a 5-wk washout period. Retrospectively, 5 apoE genotype variants were found (epsilon2/epsilon3, n = 3; epsilon3/epsilon3, n = 60; epsilon3/epsilon4, n = 23; epsilon2/epsilon4, n = 4; and epsilon4/epsilon4, n = 3). Participants were classified into the following 3 apoE phenotypes: apoE2 (n = 3), apoE3 (n = 60), and apoE4 (n = 26). Data were analyzed for apoE3 and apoE4 subgroups. Quercetin decreased systolic blood pressure by 3.4 mm Hg (P < 0.01) in the apoE3 group, whereas no significant effect was observed in the apoE4 group. Quercetin decreased serum HDL cholesterol (P < 0.01) and apoA1 (P < 0.01) and increased the LDL:HDL cholesterol ratio (P < 0.05) in the apoE4 subgroup, whereas the apoE3 subgroup had no significant changes in these variables. Quercetin significantly decreased plasma oxidized LDL and tumor necrosis factor-alpha in the apoE3 and apoE4 groups, whereas no significant inter-group differences were found. Serum C-reactive protein and nutritional status (body weight, waist circumference, fat mass, fat-free mass) were unaffected compared with placebo. In conclusion, quercetin exhibited blood pressure-lowering effects in overweight-obese carriers of the apo epsilon3/epsilon3 genotype but not in carriers of the epsilon4 allele. Furthermore, quercetin supplementation resulted in a reduction in HDL cholesterol and apoA1 in apo epsilon4 carriers.
authors.affiliation: Institute of Nutrition and Food Science, Nutritional Physiology, University of Bonn, 53115 Bonn, Germany.
authors.forename: Sarah
authors.initials: S
authors.lastname: Egert
authors.forename: Christine
authors.initials: C
authors.lastname: Boesch-Saadatmandi
authors.forename: Siegfried
authors.initials: S
authors.lastname: Wolffram
authors.forename: Gerald
authors.initials: G
authors.lastname: Rimbach
authors.forename: Manfred J
authors.initials: MJ
authors.lastname: Müller
mesh_terms: D000328:Adult; D000975:Antioxidants / Q000494:pharmacology* / Q000627:therapeutic use; D001057:Apolipoproteins E / Q000097:blood / Q000235:genetics*; D001794:Blood Pressure / Q000187:drug effects* / Q000235:genetics; D008076:Cholesterol, HDL / Q000097:blood / Q000235:genetics; D008078:Cholesterol, LDL / Q000187:drug effects / Q000235:genetics; D018592:Cross-Over Studies; D004311:Double-Blind Method; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009765:Obesity / Q000097:blood / Q000188:drug therapy / Q000235:genetics*; D010641:Phenotype; D008517:Phytotherapy; D010936:Plant Extracts / Q000494:pharmacology* / Q000627:therapeutic use; D020641:Polymorphism, Single Nucleotide; D011794:Quercetin / Q000494:pharmacology* / Q000627:therapeutic use; D014409:Tumor Necrosis Factor-alpha / Q000097:blood / Q000235:genetics
chemical_list: D000975:Antioxidants; D001057:Apolipoproteins E; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D010936:Plant Extracts; D014409:Tumor Necrosis Factor-alpha; D011794:Quercetin