title: Investigation of polymorphic variants of PPARD and APOE genes in Turkish coronary heart disease patients.
abstract: The aim of this study was to determine the role of polymorphic variants of apolipoprotein E (APOE) and peroxisome proliferator-activated receptor delta (PPARD) genes in the development of coronary heart disease (CHD), and the PPARD and APOE gene-gene interaction in a Turkish population. This study was carried out using a sample of 223 patients with CHD (103 with diabetes and 120 without diabetes) and 101 controls. PPARD +294T/C and APOE genotypes were determined by polymerase chain reaction-restriction fragment length polymorphism technique. The PPARD and APOE genotype distributions were the same between study groups (p>0.05). In the nondiabetic CHD patients, the PPARD +294 C allele showed higher serum low-density lipoprotein cholesterol (LDL-C) level than the common +294 TT homozygote genotype (3.83 ± 1.01 vs. 3.33 ± 1.14, p=0.015). In addition, a significant association between APOE 4 and PPARD +294 C alleles was detected based on their effects on LDL-C in the nondiabetic CHD patients (+294 C/APOE4: 4.43 ± 0.88 vs. +294 TT/nonAPOE 4: 3.48 ± 1.09, p = 0.009). This association indicated the interaction of two genes on plasma LDL-C levels ascended in the order +294 T<+294 T-APOE 4<+294 C<APOE 4<+294 C-APOE 4. The PPARD +294 C allele was associated with higher incidence of left ventricular hypertrophy (LVH) in all male patients with body mass index >27. In addition, the CHD patients who were +294 C allele carriers had a 2.48-fold higher risk of LVH than subjects homozygous for the T allele. An increasing effect of the PPARD +294 C allele was shown on serum LDL-C levels in nondiabetic CHD patients. In addition, the results suggested that the +294 C allele might be associated with an increased LVH risk especially in male CHD patients. Furthermore, gene-gene interaction between the PPARD +294T/C and the APOE polymorphisms was observed regarding LDL-C concentrations.
authors.affiliation: Department of Molecular Medicine, Institute for Experimental Medicine, Istanbul University, Istanbul, Turkey. hulyilmaz@yahoo.com
authors.forename: Hulya
authors.initials: H
authors.lastname: Yılmaz-Aydogan
authors.forename: Ozlem
authors.initials: O
authors.lastname: Kucukhuseyin
authors.forename: Ozlem
authors.initials: O
authors.lastname: Kurnaz
authors.forename: Basak
authors.initials: B
authors.lastname: Akadam-Teker
authors.forename: Ozlem
authors.initials: O
authors.lastname: Kurt
authors.forename: Atike
authors.initials: A
authors.lastname: Tekeli
authors.forename: Oguz
authors.initials: O
authors.lastname: Ozturk
authors.forename: Turgay
authors.initials: T
authors.lastname: Isbir
mesh_terms: D001057:Apolipoproteins E / Q000235:genetics*; D016022:Case-Control Studies; D003327:Coronary Disease / Q000235:genetics* / Q000473:pathology; D004247:DNA / Q000235:genetics; D005260:Female; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006321:Heart / Q000502:physiology; D006801:Humans; D008297:Male; D008875:Middle Aged; D047494:PPAR delta / Q000235:genetics*; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic / Q000235:genetics*; D012150:Polymorphism, Restriction Fragment Length; D011379:Prognosis; D012307:Risk Factors; D014421:Turkey
chemical_list: D001057:Apolipoproteins E; D047494:PPAR delta; D004247:DNA