The Possible Role of Mitochondrial Uncoupling Protein 2 (UCP2) Gene on the Development of Metabolic Syndrome and Platelet Count in Obese Children/Adolescents - A Preliminary Study
Nilgün Çöl Araz1, Sibel Oğuzkan Balcı2, Muradiye Nacak3, Ayşe Balat1, Sacide Pehlivan41Gaziantep University Faculty Of Medicine, Department Of Pediatrics, Gaziantep, Turkey2Gaziantep University Faculty Of Medicine, Department Of Medical Biology And Genetics, Gaziantep, Turkey
3Gaziantep University Faculty Of Medicine, Department Of Pharmacology, Gaziantep, Turkey
4Istanbul University, Istanbul Faculty Of Medicine, Department Of Medical Biology And Genetics, Istanbul, Turkey
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.
Manuscript Language: English
