title: High dietary n-6/n-3 PUFA ratio promotes HDL cholesterol level, but does not suppress atherogenesis in apolipoprotein E-null mice 1.
abstract: OBJECTIVE
  Dietary fatty acids affect atherogenesis, which was presumed to be partly related to HDL cholesterol (HDL-C) metabolism. The major aim of the work was to analyze various ratios of n-6/n-3 PUFA diets on HDL-C metabolism in apolipoprotein E-null (apoE(-/-)) mice, which have similar symptoms to human type III familial hyperlipoproteinemia.
  
  
  METHODS
  Two-month-old male apoE(-/-) mice were fed four types of n-6/n-3 PUFA diet (group 1, 1.28; group 2, 5.03; group 3, 9.98 and group 4, 68.26) and control diet, respectively, for 6 weeks. With respect to serum apolipoprotein (apo) A-I concentration, lecithin-cholesterol acyltransferase (LCAT) activity and mRNA abundance of genes involved in HDL-C metabolism in the liver were analyzed.
  
  
  RESULTS
  Group 4 diet significantly increased the plasma HDL-C and apoA-I concentrations compared with other groups. LCAT activity in serum increased with decreased ratios of n-6/n-3 PUFA. As the dietary ratio of n-6/n-3 fatty acids increased, so did mRNA levels of hepatic apoA-I, scavenger receptor B class-1 (SR-B1), LCAT, ATP binding cassette transporter A1 (ABCA1), ABCG1 and liver X receptor alpha (LXRalpha). ApoA-II mRNA level, however, had a tendency to fall. Group 4 diet increased apoA-I and ABCA1 and decreased apoA-II transcriptional levels, whereas group 1 diet decreased mRNA levels of apoA-I, LCAT, SR-B1 and ABCG1.
  
  
  CONCLUSIONS
  Our data indicated that a high ratio of n-6/n-3 PUFA increased the serum HDL-C level, but did not effectively suppress atherogenesis in apoE(-/-) mice. The elevated HDL-C level is possibly due to up-regulated hepatic apoA-I and ABCA1 with suppression of apoA-Ii expression.
authors.affiliation: The Key Laboratory of Animal Resistant Biology of Shandong, College of Life Sciences, Shandong Normal University, Jinan, PR China.
authors.forename: Liang
authors.initials: L
authors.lastname: Zhang
authors.forename: Yue
authors.initials: Y
authors.lastname: Geng
authors.forename: Ning
authors.initials: N
authors.lastname: Xiao
authors.forename: Miao
authors.initials: M
authors.lastname: Yin
authors.forename: Liufeng
authors.initials: L
authors.lastname: Mao
authors.forename: Guocheng
authors.initials: G
authors.lastname: Ren
authors.forename: Cong
authors.initials: C
authors.lastname: Zhang
authors.forename: Peng
authors.initials: P
authors.lastname: Liu
authors.forename: Nannan
authors.initials: N
authors.lastname: Lu
authors.forename: Liguo
authors.initials: L
authors.lastname: An
authors.forename: Jie
authors.initials: J
authors.lastname: Pan
mesh_terms: D000818:Animals; D001057:Apolipoproteins E / Q000172:deficiency*; D050197:Atherosclerosis / Q000517:prevention & control*; D008076:Cholesterol, HDL / Q000097:blood* / Q000378:metabolism; D004041:Dietary Fats / Q000494:pharmacology; D015525:Fatty Acids, Omega-3 / Q000494:pharmacology*; D043371:Fatty Acids, Omega-6 / Q000494:pharmacology*; D050356:Lipid Metabolism; D051379:Mice; D018345:Mice, Knockout; D014158:Transcription, Genetic / Q000187:drug effects
chemical_list: D001057:Apolipoproteins E; D008076:Cholesterol, HDL; D004041:Dietary Fats; D015525:Fatty Acids, Omega-3; D043371:Fatty Acids, Omega-6