Abstract
Aim To conduct an associative search for polymorphisms of the ACE (I/D) and PPARG (G/A), IL1RN*VNTR genes with clinical phenotypes of obesity (OB) in children.
Material and Method The study included 177 children with OB and 135 healthy children; all respondents underwent bioimpedance measurements. Testing of polymorphisms of the ACE (I/D), PPARG (G/A) and IL1RN*VNTR genes was carried out using PCR and RFLP analysis.
Results Implementation of OB in carriers of genotype ID polymorphism ACE occurs 46 times more often (OR=46.348; p=0.001). Carriage of the GG genotype of the genetic variant PPARG in OB was registered 2.8 times more often than in healthy children (OR=2.835; p=0.007). Carriage of the GG genotype of the PPARG in OB with impaired carbohydrate tolerance was recorded 3.9 times more often compared to patients with OB and normal carbohydrate metabolism (OR=3.981; p=0.014), the presence of the full complex of metabolic syndrome (MS) was observed 3.7 times more often compared to patients with OB without MS (OR=3.708; p=0.037), hypertriacylglyceremia (TAG) was recorded 4.3 times more often compared to patients with a normal lipid profile (OR= 4.398; p=0.025). Carriage of the AA genotype of the genetic variant PPARG in OB with increased skeletal muscle mass (SMM) was recorded 2.9 times more often compared to patients with OB and normal SMM (OR=2.925; p=0.044). It was found that carriers of the A1 allele of the IL1RN*VNTR gene (p=0.023) and the A1A1 genotype of the IL1RN*VNTR gene (p=0.050) are less likely to have high LDL values, according to the criteria for MS in children. It was found that among the owners of the A1 allele of the IL1RN*VNTR gene, a decrease in HDL was observed 2 times less often (p = 0.034).
Conclusions The contribution of polymorphisms of the ACE, PPARG and IL1RN*VNTR genes to the formation of clinical and metabolic phenotypes of obesity is shown.