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Provedor de dados:  Genet. Mol. Biol.
País:  Brazil
Título:  -866G/A and Ins/Del polymorphisms in the UCP2 gene and diabetic kidney disease: case-control study and meta-analysis
Autores:  Dieter,Cristine
Assmann,Taís Silveira
Lemos,Natália Emerim
Massignam,Eloísa Toscan
Souza,Bianca Marmontel de
Bauer,Andrea Carla
Crispim,Daisy
Data:  2020-01-01
Ano:  2020
Palavras-chave:  UCP2
Polymorphisms
Diabetic kidney disease
Resumo:  Abstract Uncoupling protein 2 (UCP2) decreases reactive oxygen species (ROS). ROS overproduction is a key contributor to the pathogenesis of diabetic kidney disease (DKD). Thus, UCP2 polymorphisms are candidate risk factors for DKD; however, their associations with this complication are still inconclusive. Here, we describe a case-control study and a meta-analysis conducted to investigate the association between UCP2 -866G/A and Ins/Del polymorphisms and DKD. The case-control study comprised 385 patients with type 1 diabetes mellitus (T1DM): 223 patients without DKD and 162 with DKD. UCP2 -866G/A (rs659366) and Ins/Del polymorphisms were genotyped by real-time PCR and conventional PCR, respectively. For the meta-analysis, a literature search was conducted to identify all studies that investigated associations between UCP2 polymorphisms and DKD in patients with T1DM or type 2 diabetes mellitus. Pooled odds ratios were calculated for different inheritance models. Allele and genotype frequencies of -866G/A and Ins/Del polymorphisms did not differ between T1DM case and control groups. Haplotype frequencies were also similar between groups. Four studies plus the present one were eligible for inclusion in the meta-analysis. In agreement with case-control data, the meta-analysis results showed that the -866G/A and Ins/Del polymorphisms were not associated with DKD. In conclusion, our case-control and meta-analysis studies did not indicate an association between the analyzed UCP2 polymorphisms and DKD.
Tipo:  Info:eu-repo/semantics/article
Idioma:  Inglês
Identificador:  http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1415-47572020000400101
Editor:  Sociedade Brasileira de Genética
Relação:  10.1590/1678-4685-gmb-2018-0374
Formato:  text/html
Fonte:  Genetics and Molecular Biology v.43 n.2 2020
Direitos:  info:eu-repo/semantics/openAccess
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