title: APOA1 polymorphisms are associated with variations in serum triglyceride concentrations in hypercholesterolemic individuals.
abstract: BACKGROUND
  Apolipoprotein A-I gene (APOA1) polymorphisms have been associated with variations in serum low-density lipoprotein (LDL)- and high-density lipoprotein (HDL)-cholesterol. We have investigated whether APOA1 common variants are also associated with variations in basal triglyceride serum concentrations and response to atorvastatin in individuals with hypercholesterolemia.
  
  
  METHODS
  APOA1 G-75A and C83T polymorphisms and variations in serum lipids were evaluated in 150 hypercholesterolemic (HC) and 93 normolipidemic (NL) unrelated European-derived Brazilians treated with atorvastatin (10 mg/day for 4 weeks). Genomic DNA was extracted from blood leukocytes using a salting-out method and APOA1 polymorphisms were analyzed by polymerase chain reaction and restriction fragment length polymorphism.
  
  
  RESULTS
  G-75A polymorphism was associated with differences in serum concentrations of triglyceride and very low-density lipoprotein (VLDL)-cholesterol (p=0.026) in HC men. After atorvastatin treatment, women carrying the GG/CC haplotype had lower serum triglyceride and VLDL-cholesterol (p=0.020) than non-carriers. In men, the reduction in serum triglyceride in response to atorvastatin was found to be slightly lower in GG/CC haplotype carriers (p=0.051).
  
  
  CONCLUSIONS
  Our data suggest that APOA1 polymorphisms are associated with variations of baseline serum concentrations of triglyceride and VLDL-cholesterol and in response to atorvastatin in a gender-specific manner.
authors.affiliation: Department of Clinical and Toxicological Analysis, School of Pharmaceutical Sciences, University of Sao Paulo, Sao Paulo, Brazil.
authors.forename: Simone C
authors.initials: SC
authors.lastname: Sorkin
authors.forename: Francisco J
authors.initials: FJ
authors.lastname: Forestiero
authors.forename: Mario H
authors.initials: MH
authors.lastname: Hirata
authors.forename: Elizabeth C R
authors.initials: EC
authors.lastname: Guzmán
authors.forename: Selma A
authors.initials: SA
authors.lastname: Cavalli
authors.forename: Marcelo C
authors.initials: MC
authors.lastname: Bertolami
authors.forename: Luis A
authors.initials: LA
authors.lastname: Salazar
authors.forename: Rosario D C
authors.initials: RD
authors.lastname: Hirata
mesh_terms: D016632:Apolipoprotein A-I / Q000235:genetics*; D000069059:Atorvastatin; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D015243:Cholesterol, VLDL / Q000097:blood; D005260:Female; D014644:Genetic Variation; D023281:Genomics; D006239:Haplotypes; D006538:Heptanoic Acids / Q000494:pharmacology / Q000627:therapeutic use; D006801:Humans; D006937:Hypercholesterolemia / Q000235:genetics* / Q000378:metabolism; D008297:Male; D011110:Polymorphism, Genetic; D011758:Pyrroles / Q000494:pharmacology / Q000627:therapeutic use; D012737:Sex Factors; D016896:Treatment Outcome; D014280:Triglycerides / Q000097:blood*
chemical_list: D016632:Apolipoprotein A-I; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D015243:Cholesterol, VLDL; D006538:Heptanoic Acids; D011758:Pyrroles; D014280:Triglycerides; D000069059:Atorvastatin