No evidence for involvement of the promoter polymorphism -: 866 G/A of the UCP2 gene in childhood-onset obesity in humans
No evidence for involvement of the promoter polymorphism -: 866 G/A of the UCP2 gene in childhood-onset obesity in humans
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DOI:
10.1055/s-2003-39232
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发表时间:
2003-04-01
影响因子:
1.8
通讯作者:
Hebebrand, J
中科院分区:
文献类型:
--
作者:
Schäuble, N;Geller, F;Hebebrand, J
Recently, an association between obesity and the G-allele of the - 866 G/A polymorphism in the promoter region of uncoupling protein-2 gene (UCP2) was reported. Both allele frequencies and genotype distributions for this polymorphism differed between obese individuals and never-obese controls.We attempted to confirm this finding. Genotyping was performed by polymerase chain reaction with subsequent restriction fragment length polymorphism analysis (PCR-RFLP).We analysed transmission disequilibrium of the (wild type) G-allele for 200 extremely obese children and adolescents from 93 concordant sib pair families using the pedigree disequilibrium test. Additionally, using a one-sided asymptotic Pearson's chi(2)-test, we tested whether the G-allele occurs more frequently in 277 extremely obese children and adolescents (including the 93 index patients of the concordant sib pairs) than in 188 never-obese controls. The one-sided asymptotic Cochran Armitage trend test was used to determine differences in genotype frequencies between extremely obese and healthy underweight individuals. The PDT analysis revealed no evidence for transmission disequilibrium in obesity. Allele and genotype frequencies did not differ between the extremely obese and never-obese subjects. In conclusion, we cannot confirm the results of Esterbauer et al. (2001) in our young sample.