title: Effects of dietary maritime pine (Pinus pinaster)-seed oil on high-density lipoprotein levels and in vitro cholesterol efflux in mice expressing human apolipoprotein A-I.
abstract: Maritime pine (Pinus pinaster)-seed oil contains two Delta5 unsaturated polymethylene interrupted fatty acids (all cis-5,9, 12-18:3 and all cis-5,11,14-20:3 acids) one of which resembles eicosapentaenoic acid. The goal of the present study was to test whether maritime pine-seed oil consumption affects HDL and apolipoprotein (Apo) A-I levels as well as the ability of serum to promote efflux of cholesterol from cultured cells. To this end, wild type (WT) non-transgenic mice and transgenic mice expressing human ApoA-I (HuA-ITg) were fed on isoenergetic diet containing either 200 g maritime pine-seed oil/kg or 200 g lard/kg for 2 weeks. WT and HuA-ITg mice fed maritime pine-seed oil had lower cholesterol, HDL-cholesterol, LDL-cholesterol and HuA-ITg mice had lower human ApoA-I than those fed lard. The differences in cholesterol (P < 0.0001) and HDL-cholesterol (P < 0.003) levels between mice fed on the two diets were more pronounced in the HuA-ITg than in the WT mice. The ability of HuA-ITg serum to promote cholesterol efflux in cultured cells was greater (P < 0.008) than that of WT animals. However, the maritime pine-seed oil diet was associated with lower (P < 0.005) in vitro cholesterol efflux ability than the lard diet in both mice genotypes. This suggests a negative effect of the maritime pine-seed oil on reverse cholesterol transport. Cholesterol efflux was correlated with serum free or esterified cholesterol and phospholipid levels. The slope of the regression line was smaller in the HuA-ITg than in the WT mice indicating that overexpression of human ApoA-I reduces the negative impact of maritime pine-seed oil on cholesterol efflux. In conclusion, maritime pine-seed oil diet lowers HDL-cholesterol and diminishes in vitro cholesterol efflux. This potentially detrimental effect is attenuated by overexpression of human ApoA-I in mice.
authors.affiliation: INSERM U-325, Departement d'Atherosclerose, Institut Pasteur de Lille, 1 rue de Professeur Calmette, 59019 Lille Cedex, France.
authors.forename: G
authors.initials: G
authors.lastname: Asset
authors.forename: A
authors.initials: A
authors.lastname: Leroy
authors.forename: E
authors.initials: E
authors.lastname: Bauge
authors.forename: R L
authors.initials: RL
authors.lastname: Wolff
authors.forename: J C
authors.initials: JC
authors.lastname: Fruchart
authors.forename: J
authors.initials: J
authors.lastname: Dallongeville
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D016632:Apolipoprotein A-I / Q000235:genetics / Q000378:metabolism*; D002784:Cholesterol / Q000378:metabolism*; D004042:Dietary Fats, Unsaturated / Q000008:administration & dosage / Q000494:pharmacology; D006801:Humans; D008075:Lipoproteins, HDL / Q000378:metabolism*; D051379:Mice; D008810:Mice, Inbred C57BL; D010938:Plant Oils / Q000008:administration & dosage / Q000494:pharmacology*
chemical_list: D016632:Apolipoprotein A-I; D004042:Dietary Fats, Unsaturated; D008075:Lipoproteins, HDL; D010938:Plant Oils; D002784:Cholesterol