Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/77694
Type: Artigo de periódico
Title: Toll-like receptor 4 and inducible nitric oxide synthase gene polymorphisms are associated with Type 2 diabetes
Author: Bagarolli, RA
Saad, MJA
Saad, STO
Abstract: Background: The toll-like receptor 4 (TLR4) and inducible nitric oxide synthase are proteins from the innate immune system that, when activated, can induce insulin resistance. Polymorphisms in these genes, TLR4 and NOS2, respectively, could affect the immune response, as well as the prevalence of Type 2 diabetes (T2DM). Objective: The aim of the present study was to investigate the contribution of four polymorphisms (two from TLR4 and two from NOS2) to susceptibility to T2DM in a southeast Brazilian population. Design: A total of 211 patients with T2DM and 200 unrelated controls were genotyped for the Asp299Gly and Thr399Ile polymorphisms of the TLR4 gene and for the insertion (1)/deletion (D) AAAT and (CCTTT)n polymorphisms of the NOS2 promoter gene. Results: With regard to the NOS2 promoter region, the data showed that the I allele of the I/D AAAT polymorphism was more prevalent in the T2DM group and that the L/L genotype of the (CCTTT)n polymorphism was also more frequent in the same group. In contrast, the 299Gly allele and the 399Ile allele from the Asp299Gly and Thr399Ile TLR4 gene polymorphisms, respectively, were associated with protection of T2DM. It is believed that the persistence of these genetic variations in human populations may be indicative of a selective advantage in the face of different environmental pressures. Conclusions: Genetic variations in the NOS2 gene promoter and TLR4 coding sequence may lead to deleterious and protective effects, respectively, arising from altered function of the innate immune system in patients with T2DM. (C) 2010 Elsevier Inc. All rights reserved.
Subject: Type 2 diabetes
iNOS
TLR4
Polymorphism
Country: EUA
Editor: Elsevier Science Inc
Rights: fechado
Identifier DOI: 10.1016/j.jdiacomp.2009.03.003
Date Issue: 2010
Appears in Collections:Unicamp - Artigos e Outros Documentos

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