Data/hora: 03/06/2024 02:36:28

Provedor de dados: 	74	
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	
Fonte: 	info:eu-repo/semantics/openAccess