Association of PPAR Alpha Intron 7 G/C, PPAR Gamma 2 Pro12Ala, and C161T Polymorphisms with Serum Fetuin-A Concentrations

• Main Authors: Bernadett Márkus, Krisztián Vörös, Dorina Supák, Zsolt Melczer, Károly Cseh, László Kalabay
• Format: Article
• Language: English
• Published: Hindawi Limited 2017-01-01
• Series: PPAR Research
• Online Access: http://dx.doi.org/10.1155/2017/7636019

Background. Both peroxisome activator proteins (PPARs) and fetuin-A play a role in lipid and glucose metabolism. Aims. We investigated whether PPARα intron 7 G2468/C and PPARγ2 Pro12Ala and PPARγ exon 6 C161T polymorphisms are associated with serum fetuin-A concentrations. Patients and Methods. The PPARα intron 7 G/C polymorphism was studied in cohort 1 (79 reference individuals, 165 postinfarction patients). The two PPARγ polymorphisms were investigated in cohort 2 (162 reference individuals, 165 postinfarction patients). Fetuin-A levels and PPAR polymorphisms were determined by radial immunodiffusion and polymerase chain reaction-restriction fragment length polymorphism techniques. Results. The C allele variant of PPARα intron 7 G2467C was associated with higher fetuin-A levels (p=0.018). Postinfarction status (p=0.001), PPARα intron 7 GG/GC/CC genotypes (p=0.032), and the C allele (p=0.021) were the strongest determinants of fetuin-A concentration in a multiple regression model. Higher fetuin-A levels were associated with the Pro variant of PPARγ2 (p=0.047). Postinfarction status (p=0.041) and BMI (p<0.001) but not PPARγ2 Pro were the strongest determinants of fetuin-A concentrations. PPARγ exon 6 C161T genotypes were not associated with fetuin-A levels. Conclusions. Fetuin-A was determined mainly by the PPARα intron 7C allele and postinfarction status in cohort 1 and the BMI and postinfarction in cohort 2. The PPARα intron 7C and PPARγ2 Pro variants are associated with fetuin-A levels.