title: Different effects of PPARA, PPARG and ApoE SNPs on serum lipids in patients with coronary heart disease based on the presence of diabetes.
abstract: BACKGROUND
  The aim of this study was to investigate the individual or combined effects of PPARA-L162V, PPARG-C161T and APOE polymorphisms on hyperlipidemia in coronary heart disease (CHD) patients.
  
  
  METHODS
  Our study included 223 patients with CHD (103 with type 2 diabetes (T2DM), 120 without diabetes) and 101 controls. All genotypes were determined by PCR-RFLP technique.
  
  
  RESULTS
  Genotypic and allelic distributions of PPARA-L162V polymorphism were similar between study and control groups (p>0.05). The serum total-cholesterol (TC) and LDL-cholesterol (LDL-C) levels were higher in PPARA-V162 allele carriers in non-diabetic CHD patients (p=0.007 and p=0.038, respectively). The increasing effect of the PPARA-V162 allele on serum TC and LDL-C levels was weakened with the presence of PPARG-161T allele in the non-diabetic CHD patients. The ApoE4-PPARA-V162 allelic combination of the ApoE/PPARA genes was found to be more frequent in diabetic CHD patients independent of serum lipids (p=0.035).
  
  
  CONCLUSIONS
  The PPARA V162 allele has an increasing effect on TC and LDL-C levels and this effect was reduced by carrying PPARG T161 allele in non-diabetic CHD patients. On the other hand, the V162 allele may be associated with an increased risk of CHD in diabetic CHD patients due to the presence of ApoE4 allele independent of serum lipids. We suggest that the PPARA L162V polymorphism may have diverse effects on serum lipids and CHD risk depends on the presence of T2DM.
authors.affiliation: Department of Molecular Medicine, The Institute of Experimental Medicine, Istanbul University, Istanbul, Turkey. hulyilmaz@yahoo.com
authors.forename: Hulya
authors.initials: H
authors.lastname: Yilmaz-Aydogan
authors.forename: Ozlem
authors.initials: O
authors.lastname: Kurnaz
authors.forename: Ozlem
authors.initials: O
authors.lastname: Kucukhuseyin
authors.forename: Basak
authors.initials: B
authors.lastname: Akadam-Teker
authors.forename: Ozlem
authors.initials: O
authors.lastname: Kurt
authors.forename: Allison Pinar
authors.initials: AP
authors.lastname: Eronat
authors.forename: Atike
authors.initials: A
authors.lastname: Tekeli
authors.forename: Zehra
authors.initials: Z
authors.lastname: Bugra
authors.forename: Oguz
authors.initials: O
authors.lastname: Ozturk
mesh_terms: D000328:Adult; D000368:Aged; D000483:Alleles; D053327:Apolipoprotein E4 / Q000235:genetics* / Q000378:metabolism; D016022:Case-Control Studies; D002784:Cholesterol / Q000097:blood; D003327:Coronary Disease / Q000097:blood / Q000235:genetics* / Q000473:pathology; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000235:genetics / Q000473:pathology*; D005260:Female; D005787:Gene Frequency; D056726:Genetic Association Studies; D020022:Genetic Predisposition to Disease; D006801:Humans; D006937:Hypercholesterolemia / Q000097:blood / Q000235:genetics / Q000473:pathology; D008297:Male; D008875:Middle Aged; D047493:PPAR alpha / Q000235:genetics*; D047495:PPAR gamma / Q000235:genetics*; D016133:Polymerase Chain Reaction; D012150:Polymorphism, Restriction Fragment Length; D020641:Polymorphism, Single Nucleotide; D012307:Risk Factors; D014421:Turkey
chemical_list: D053327:Apolipoprotein E4; D047493:PPAR alpha; D047495:PPAR gamma; D002784:Cholesterol