Álvaro Hernáez1, Sara Fernández-Castillejo1, Marta Farràs1, Úrsula Catalán1, Isaac Subirana1, Rosa Montes1, Rosa Solà1, Daniel Muñoz-Aguayo1, Anna Gelabert-Gorgues1, Óscar Díaz-Gil1, Kristiina Nyyssönen1, Hans-Joachim F Zunft1, Rafael de la Torre1, Sandra Martín-Peláez1, Anna Pedret1, Alan T Remaley1, María-Isabel Covas1, Montserrat Fitó2. 1. From the Cardiovascular Risk and Nutrition Research Group, REGICOR Study Group, CIBER de Fisiopatología de la Nutrición y la Obesidad (CIBEROBN) (A.H., M.F., D.M.-A., A.G.-G., O.D.-G., S.M.-P., M.-I.C., M.F.), Cardiovascular Epidemiology and Genetics Research Group, REGICOR Study Group, CIBER de Epidemiología y Salud Pública (CIBERESP) (I.S.), and Human Pharmacology and Clinical Neurosciences Research Group (R.d.l.T.), IMIM-Research Institute Hospital del Mar, Barcelona, Spain; Ph.D program of Food Sciences and Nutrition (A.H.) and Department of Nutrition and Bromatology, Faculty of Pharmacy (R.M.), Universitat de Barcelona, Barcelona, Spain; Research Unit on Lipids and Atherosclerosis, Hospital Universitari Sant Joan, IISPV, Universitat Rovira I Virgili and CIBER de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Reus, Spain (S.F.-C., U.C., R.S., A.P.); Ph.D program in Biochemistry, Molecular Biology and Biomedicine, Department of Biochemistry and Molecular Biology, Universitat Autònoma de Barcelona, Barcelona, Spain (M.F.); Institute of Public Health and Clinical Nutrition, University of Eastern Finland, Kuopio, Finland (K.N.); German Institute of Human Nutrition (DIFE), Potsdam-Rehbruecke, Germany (H.-J.F.Z.); and Lipoprotein Metabolism Section, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD (A.T.R.). 2. From the Cardiovascular Risk and Nutrition Research Group, REGICOR Study Group, CIBER de Fisiopatología de la Nutrición y la Obesidad (CIBEROBN) (A.H., M.F., D.M.-A., A.G.-G., O.D.-G., S.M.-P., M.-I.C., M.F.), Cardiovascular Epidemiology and Genetics Research Group, REGICOR Study Group, CIBER de Epidemiología y Salud Pública (CIBERESP) (I.S.), and Human Pharmacology and Clinical Neurosciences Research Group (R.d.l.T.), IMIM-Research Institute Hospital del Mar, Barcelona, Spain; Ph.D program of Food Sciences and Nutrition (A.H.) and Department of Nutrition and Bromatology, Faculty of Pharmacy (R.M.), Universitat de Barcelona, Barcelona, Spain; Research Unit on Lipids and Atherosclerosis, Hospital Universitari Sant Joan, IISPV, Universitat Rovira I Virgili and CIBER de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Reus, Spain (S.F.-C., U.C., R.S., A.P.); Ph.D program in Biochemistry, Molecular Biology and Biomedicine, Department of Biochemistry and Molecular Biology, Universitat Autònoma de Barcelona, Barcelona, Spain (M.F.); Institute of Public Health and Clinical Nutrition, University of Eastern Finland, Kuopio, Finland (K.N.); German Institute of Human Nutrition (DIFE), Potsdam-Rehbruecke, Germany (H.-J.F.Z.); and Lipoprotein Metabolism Section, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD (A.T.R.). mfito@imim.es.
Abstract
OBJECTIVE:Olive oil polyphenols have shown beneficial properties against cardiovascular risk factors. Their consumption has been associated with higher cholesterol content in high-density lipoproteins (HDL). However, data on polyphenol effects on HDL quality are scarce. We, therefore, assessed whether polyphenol-rich olive oil consumption could enhance the HDL main function, its cholesterol efflux capacity, and some of its quality-related properties, such HDL polyphenol content, size, and composition. APPROACH AND RESULTS: A randomized, crossover, controlled trial with 47 healthy European male volunteers was performed. Participants ingested 25 mL/d of polyphenol-poor (2.7 mg/kg) or polyphenol-rich (366 mg/kg) raw olive oil in 3-week intervention periods, preceded by 2-week washout periods. HDL cholesterol efflux capacity significantly improved after polyphenol-rich intervention versus the polyphenol-poor one (+3.05% and -2.34%, respectively; P=0.042). Incorporation of olive oil polyphenol biological metabolites to HDL, as well as large HDL (HDL2) levels, was higher after the polyphenol-rich olive oil intervention, compared with the polyphenol-poor one. Small HDL (HDL3) levels decreased, the HDL core became triglyceride-poor, and HDL fluidity increased after the polyphenol-rich intervention. CONCLUSIONS:Olive oil polyphenols promote the main HDL antiatherogenic function, its cholesterol efflux capacity. These polyphenols increased HDL size, promoted a greater HDL stability reflected as a triglyceride-poor core, and enhanced the HDL oxidative status, through an increase in the olive oil polyphenol metabolites content in the lipoprotein. Our results provide for the first time a first-level evidence of an enhancement in HDL function by polyphenol-rich olive oil.
RCT Entities:
OBJECTIVE:Olive oil polyphenols have shown beneficial properties against cardiovascular risk factors. Their consumption has been associated with higher cholesterol content in high-density lipoproteins (HDL). However, data on polyphenol effects on HDL quality are scarce. We, therefore, assessed whether polyphenol-rich olive oil consumption could enhance the HDL main function, its cholesterol efflux capacity, and some of its quality-related properties, such HDL polyphenol content, size, and composition. APPROACH AND RESULTS: A randomized, crossover, controlled trial with 47 healthy European male volunteers was performed. Participants ingested 25 mL/d of polyphenol-poor (2.7 mg/kg) or polyphenol-rich (366 mg/kg) raw olive oil in 3-week intervention periods, preceded by 2-week washout periods. HDL cholesterol efflux capacity significantly improved after polyphenol-rich intervention versus the polyphenol-poor one (+3.05% and -2.34%, respectively; P=0.042). Incorporation of olive oil polyphenol biological metabolites to HDL, as well as large HDL (HDL2) levels, was higher after the polyphenol-rich olive oil intervention, compared with the polyphenol-poor one. Small HDL (HDL3) levels decreased, the HDL core became triglyceride-poor, and HDL fluidity increased after the polyphenol-rich intervention. CONCLUSIONS:Olive oil polyphenols promote the main HDL antiatherogenic function, its cholesterol efflux capacity. These polyphenols increased HDL size, promoted a greater HDL stability reflected as a triglyceride-poor core, and enhanced the HDL oxidative status, through an increase in the olive oil polyphenol metabolites content in the lipoprotein. Our results provide for the first time a first-level evidence of an enhancement in HDL function by polyphenol-rich olive oil.
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