Key result
The interaction between PPARγ Pro12Ala or Ala12Ala and LPL Pvu (-/+) or (+/+) genotypes significantly increased the odds of metabolic syndrome (OR 5.98; 95% CI 1.46-24.47; P=0.013).
Case-Control (n=527)
Effect estimate: OR 5.98 (95% CI 1.46-24.47)
p-value: p=0.013
Interactions between PPARγ gene variants and target genes like LPL, IL6, and ACE significantly modulate the risk of developing metabolic syndrome and its individual traits.
Gene interactions may elevate metabolic syndrome risk; hypothesis-generating and requires prospective validation before clinical use.
AIM: The aim of the study was to estimate the influence of interactions between peroxisome proliferator-activated receptor γ (PPARγ) and target genes lipoprotein lipase (LPL), interleukin 6 (IL6), angiotensin converting enzyme (ACE), and angiotensin II type 1 receptor (AT1R) on metabolic syndrome (MetSy) and its traits. METHODS: The 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 polymerase chain reaction-restriction fragment length polymorphism-based methods. RESULTS: Interaction between PPARγ Pro12Ala and LPL Pvu(-/+) improved prediction of MetSy over and above prediction based on a model containing no interactions (χ(2)=7.22; df=1; p=0.007). In the group of participants with PPARγ Pro12Ala or Ala12Ala genotypes, those with the LPL Pvu (-/+) or (+/+) genotype had greater odds for MetSy (odds ratio OR=5.98; 95% confidence interval CI: 1.46-24.47, p=0.013). Interaction between PPARγ Pro12Ala and IL6 -174G>C improved prediction of high fasting blood glucose (χ(2)=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 with 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.
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Božina et al. (2013) conducted a case-control in Metabolic syndrome (MetSy) (n=527). Genetic interactions (PPARγ and target genes LPL, IL6, ACE, AT1R) vs. Alternative genotypes / Controls was evaluated on Metabolic syndrome (MetSy) (OR 5.98, 95% CI 1.46-24.47, p=0.013). The interaction between PPARγ Pro12Ala or Ala12Ala and LPL Pvu (-/+) or (+/+) genotypes significantly increased the odds of metabolic syndrome (OR 5.98; 95% CI 1.46-24.47; P=0.013).
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