title: The peroxisome proliferator-activated receptor alpha Leu162Val polymorphism influences the metabolic response to a dietary intervention altering fatty acid proportions in healthy men.
abstract: BACKGROUND
  Serum lipid responses to dietary modification are partly determined by genetic factors.
  
  
  OBJECTIVE
  We tested whether plasma lipoprotein and lipid responsiveness to a modification in the dietary ratio of polyunsaturated to saturated fatty acids (P:S) is influenced by the peroxisome proliferator-activated receptor alpha (PPARalpha) Leu162Val polymorphism in healthy men.
  
  
  METHODS
  Ten carriers of the V162 allele and 10 L162 homozygotes were matched according to age and body mass index (BMI). During the protocol, all subjects followed the National Cholesterol Education Program Step I diet, but intake of saturated and polyunsaturated fatty acids was adjusted to obtain a P:S of 0.3 for the first 4-wk period (low-P:S diet) and a P:S of 1.0 for the next 4-wk period (high-P:S diet).
  
  
  RESULTS
  At screening, the PPARalpha Leu162Val polymorphism was not associated with anthropometric indexes or plasma lipoprotein and lipid concentrations. After the high-P:S diet, a significant gene-by-diet interaction was observed for changes in plasma total cholesterol, apolipoprotein (apo) A-I, and cholesterol concentrations in small LDL particles (P <or= 0.05). Mean differences after the high-P:S diet were observed between genotype groups for plasma apo A-I concentrations (P<0.05). Changes in BMI, waist circumference, and concentrations of triacylglycerol, phospholipid, and apo B did not differ significantly between groups.
  
  
  CONCLUSIONS
  The PPARalpha Leu162Val polymorphism may contribute to interindividual variability in plasma lipoprotein and lipid response after modification of the dietary P:S ratio.
authors.affiliation: Lipid Research Center and the Molecular Endocrinology and Oncology Laboratory Research Center, CHUQ-CHUL Pavilion, Sainte-Foy, Canada.
authors.forename: Ann-Marie
authors.initials: AM
authors.lastname: Paradis
authors.forename: Bénédicte
authors.initials: B
authors.lastname: Fontaine-Bisson
authors.forename: Yohan
authors.initials: Y
authors.lastname: Bossé
authors.forename: Julie
authors.initials: J
authors.lastname: Robitaille
authors.forename: Simone
authors.initials: S
authors.lastname: Lemieux
authors.forename: Hélène
authors.initials: H
authors.lastname: Jacques
authors.forename: Benoît
authors.initials: B
authors.lastname: Lamarche
authors.forename: André
authors.initials: A
authors.lastname: Tchernof
authors.forename: Patrick
authors.initials: P
authors.lastname: Couture
authors.forename: Marie-Claude
authors.initials: MC
authors.lastname: Vohl
mesh_terms: D000328:Adult; D000483:Alleles; D000886:Anthropometry; D016632:Apolipoprotein A-I / Q000097:blood*; D002784:Cholesterol / Q000097:blood* / Q000378:metabolism; D002791:Cholesterol, Dietary / Q000008:administration & dosage; D008078:Cholesterol, LDL / Q000737:chemistry; D005227:Fatty Acids / Q000008:administration & dosage*; D005231:Fatty Acids, Unsaturated / Q000008:administration & dosage*; D005787:Gene Frequency; D005838:Genotype; D006801:Humans; D008297:Male; D008875:Middle Aged; D047493:PPAR alpha / Q000235:genetics* / Q000378:metabolism; D012150:Polymorphism, Restriction Fragment Length
chemical_list: D016632:Apolipoprotein A-I; D002791:Cholesterol, Dietary; D008078:Cholesterol, LDL; D005227:Fatty Acids; D005231:Fatty Acids, Unsaturated; D047493:PPAR alpha; D002784:Cholesterol