Effects of the PPARG P12A and C161T gene variants on serum lipids in coronary heart disease patients with and without Type 2 diabetes

• Published in: Molecular and cellular biochemistry Vol. 358; no. 1-2; pp. 355 - 363
• Main Authors: Yilmaz-Aydogan, Hulya, Kurnaz, Ozlem, Kurt, Ozlem, Akadam-Teker, Basak, Kucukhuseyin, Ozlem, Tekeli, Atike, Isbir, Turgay
• Format: Journal Article
• Language: English
• Published: Boston Springer US 01.12.2011; Springer; Springer Nature B.V
• Subjects: Alleles; Amino Acid Substitution - genetics; Biochemistry; Biomedical and Life Sciences; Blood lipids; Cardiology; Cardiovascular disease; Cardiovascular diseases; Cholesterol; Comparative analysis; Coronary Disease - blood; Coronary Disease - complications; Coronary Disease - genetics; Coronary heart disease; Demography; Diabetes; Diabetes mellitus; Diabetes Mellitus, Type 2 - blood; Diabetes Mellitus, Type 2 - complications; Diabetes Mellitus, Type 2 - genetics; Diabetes therapy; Diabetics; Female; Gene polymorphism; Genes; Genetic Predisposition to Disease; Genetics; Genotypes; Heterozygotes; Homozygotes; Humans; Life Sciences; Lipid Metabolism - genetics; Lipids; Lipids - blood; Male; Medical Biochemistry; Middle Aged; Oncology; Peroxisome proliferator-activated receptors; Polymerase chain reaction; Polymorphism; Polymorphism, Single Nucleotide - genetics; PPAR gamma - genetics; Restriction fragment length polymorphism; Serum lipids; Triglycerides; Triglycerides - blood; Type 2 diabetes; Lipids; PPARG; Diabetes; Coronary heart disease; Polymorphism
• ISSN: 0300-8177; 1573-4919
• DOI: 10.1007/s11010-011-0987-y

We investigated whether PPAR-γ2 gene polymorphisms are associated with serum lipids and the occurrence of coronary heart disease (CHD) prospectively characterised for the presence or absence of Type 2 diabetes in a Turkish population. Our study included 202 patients with CHD (102 with diabetes, 100 without diabetes) and 105 controls. PPARγ genotypes were determined by PCR-RFLP technique. The PPARγ-C161T CC homozygote genotype was associated with significantly increased CHD risk when compared with the T allele carriers (CT+TT) in CHD patients with diabetes (OR:1.951, 95%CI: 1.115–3.415, P  = 0.019), whereas PPARγ-P12A polymorphism was not associated with CHD risk ( P  > 0.05). Serum HDL-C levels were significantly lower in controls with the P12A heterozygote when compared with the P12P homozygote ( P  = 0.002). In the CHD patients with diabetes, CT heterozygote genotype showed higher serum triglyceride than the CC homozygote genotype (CT:2.42 ± 1.89 vs. CC:1.61 ± 0.21, P  = 0.015). Our findings shows the association of these two polymorphisms with serum triglyceride levels, which was increased in the order of P12P-CC < P12P-CT < P12A-CC < P12A-CT in the CHD patients with diabetes. Furthermore, we observed that the increasing effects of the CT genotype on serum triglyceride levels could be modified by PPARγ P12A polymorphism (P12A-CT:2.30 ± 1.75 vs. P12P-CC:1.79 ± 1.14, P  = 0.028). We suggested that homozygote CC genotype of the PPARγ C161T polymorphism might be associated with an increased CHD risk especially in patients with diabetes. We observed that the C161T CT heterozygote genotype shows an unfavorable effect on serum lipid profile in CHD patients with diabetes and this effect was weaken with the presence of P12P homozygote genotype.