title: A diet enriched in monounsaturated fats decreases low density lipoprotein concentrations in cynomolgus monkeys by a different mechanism than does a diet enriched in polyunsaturated fats.
abstract: To determine the mechanisms whereby dietary fat saturation influences LDL cholesterol and apolipoprotein B concentrations, 10 cynomolgus monkeys were fed each of three experimental diets enriched in saturated, monounsaturated or polyunsaturated fatty acids in a crossover design consisting of three 13-wk periods. Each diet contained 30% of energy as fat with 0.05 mg cholesterol/kJ and differed solely by the isocaloric substitution of fatty acids as 60% of total fat energy. The replacement of dietary saturated fatty acids with either mono- or polyunsaturated fatty acids resulted in significant reductions of plasma total cholesterol (-17% and -30%, respectively), HDL cholesterol (-32% and -41%, respectively), apoA-1 (-37% and -44%, respectively), and apolipoprotein B (-28% and -36%, respectively) concentrations. Additionally, when dietary polyunsaturated fatty acids were substituted for saturated fatty acids, a 27% reduction in VLDL + LDL cholesterol was significant. Metabolic experiments suggested that the significantly reduced concentrations of apolipoprotein B observed during the monounsaturated and polyunsaturated fatty acid phases relative to the saturated fatty acid phase could not be entirely explained by changes in LDL apolipoprotein B clearance but rather were likely due to decreased LDL apolipoprotein B production rates. However, enhanced LDL apolipoprotein B catabolism accounted for the even greater reductions in VLDL + LDL cholesterol and apolipoprotein B concentrations observed during the polyunsaturated fatty acid phase vs. the monounsaturated fatty acid phase. Our data suggest that monounsaturated and polyunsaturated fatty acids lower apolipoprotein B concentrations by distinct mechanisms, with polyunsaturated fatty acids affecting LDL apolipoprotein B catabolism as well as production.
authors.affiliation: Department of Clinical Sciences, University of Massachusetts-Lowell.
authors.forename: M E
authors.initials: ME
authors.lastname: Brousseau
authors.forename: A F
authors.initials: AF
authors.lastname: Stucchi
authors.forename: D B
authors.initials: DB
authors.lastname: Vespa
authors.forename: E J
authors.initials: EJ
authors.lastname: Schaefer
authors.forename: R J
authors.initials: RJ
authors.lastname: Nicolosi
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D016632:Apolipoprotein A-I / Q000032:analysis; D001055:Apolipoproteins B / Q000032:analysis / Q000378:metabolism; D002784:Cholesterol / Q000097:blood; D004041:Dietary Fats / Q000494:pharmacology*; D005229:Fatty Acids, Monounsaturated / Q000008:administration & dosage / Q000494:pharmacology*; D005231:Fatty Acids, Unsaturated / Q000008:administration & dosage / Q000494:pharmacology*; D008077:Lipoproteins, LDL / Q000097:blood* / Q000737:chemistry / Q000187:drug effects; D008252:Macaca fascicularis; D008297:Male; D014280:Triglycerides / Q000097:blood
chemical_list: D016632:Apolipoprotein A-I; D001055:Apolipoproteins B; D004041:Dietary Fats; D005229:Fatty Acids, Monounsaturated; D005231:Fatty Acids, Unsaturated; D008077:Lipoproteins, LDL; D014280:Triglycerides; D002784:Cholesterol