Introduction: The aim of this study was to determine the potential relationship between polymorphisms of the uncoupling protein 2 (UCP2) gene and metabolic syndrome (MS) and platelet count in obese children/adolescents.
Method: One-hundred unrelated obese children and adolescents (57 of them with MS) were selected. MS was defined according to the “National Cholesterol Education Program” criteria. The -866G >A and 45 bp insertion/deletion (I/D) polymorphisms of the human UCP2 gene were genotyped using the polymerase chain reaction-restriction fragment length polymorphism method. A p-value <0.05 was considered statistically significant.
Results: The mean age of 100 obese patients (55 male/45 female) was 11.32±3.82 years (range 3-17 years). For the -866 G>A polymorphism, the distributions of G/G, G/A, and A/A genotypes were respectively 22.8%, 49.1%, and 28.1% in patients with MS compared to 9.3%, 60.5%, and 30.2% in patients without MS (p>0.05). The allele frequencies of G and A were 47.4% and 52.6% in patients with MS and 39.5% and 60.5% in patients without MS (p>0.05). The distributions of D/D, D/I, and I/I genotypes for the I/D polymorphism were 52.6%, 24.6%, and 22.8% in patients with MS compared to 37.2%, 39.5%, and 23.3% in patients without MS (p>0.05). The allele frequencies of D and I were 64.9% and 35.1% in patients with MS and 57.0% and 43.0% in patients without MS (p>0.05). Platelet count was found significantly higher in patients with MS carrying I allele (p=0.004).
Conclusion: This study could not verify the potential role of UCP2 gene polymorphisms on the development of MS in childhood obesity. However, I allele of UCP2 gene may have a possible role, as a risk factor, in the development of atherothrombosis in obese children with MS. Since this is a preliminary study, further investigations with larger populations are needed to confirm the exact role(s) of this gene in obese children.