engleski

Interaction of Genetic Risk Factors Confers Increased Risk for Metabolic Syndrome : The Role of Peroxisome Proliferator-Activated Receptor γ

The aim of the study was to estimate the influence of interactions between PPARγ and target genes LPL, IL6, ACE and AT1R on metabolic syndrome (MetSy) and its traits. Methods: Study included 527 participants (263 with MetSy and 264 controls). Genotyping of PPARγ Pro12Ala, LPL PvuII (-/+), IL6 -174G>C, ACE I/D and AT1R 1166A>C was performed using PCR-RFLP based methods. Results: Interaction between PPARγ Pro12Ala and LPL (Pvu-/+) improved prediction of MetSy over and above prediction based on model containing no interactions (χ2=7.22 ; df=1 ; p=0.007). In the group of participants with PPARγ Pro12Ala or Ala12Ala genotypes, those with LPL Pvu (-/+) or (+/+) genotype had greater odds for MetSy (OR=5.98 ; 95% CI: 1.46-24.47, p=0.013). Interaction between PPARγ Pro12Ala and IL6 -174G>C improved prediction of high fasting blood glucose (χ2=13.99 ; df=1 ; p<0.001). PPARγ Ala12 variant was found protective in patients with IL6 -174GG genotype (OR=0.10 ; 95% CI: 0.02-0.57, p=0.01), while in the case of IL6 -174C allele carriers, for PPARγ Ala12 carriers larger odds for high glucose levels compared to Pro12 variant were observed (OR=2.39 ; 95% CI: 1.11-5.17, p=0.026). Interactions of PPARγ and ACE were significant for BMI. In the group with ACE DD genotype, those with PPARγ Pro12Ala or Ala12Ala genotype have greater odds for obesity (OR=9.98 ; 95% CI: 1.18-84.14, p=0.034). Conclusions: PPARγ gene variants can, in interaction with some of its target genes, modulate physiological processes leading to the development of MetSy.

metabolic syndrome; genetic polymorphisms; peroxisome proliferator-activated receptor γ gene; lipoprotein lipase; interleukin 6; angiotensin converting enzyme; angiotensin II type 1 receptor

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