Alvim, Rafael de OliveiraSantos, Paulo Caleb Júnior de LimaNascimento Neto, Raimundo Marques doCoelho, George Luiz Lins MachadoMill, José GeraldoKrieger, José EduardoPereira, Alexandre da Costa2014-11-122014-11-122012ALVIM. R. O. et al. BDKRB2 +9/−9 polymorphism Is associated with higher risk for diabetes mellitus in the Brazilian general population. Experimental Diabetes Research, v. 2012, p. 1-4, 2012. Disponível em: <http://www.hindawi.com/journals/jdr/2012/480251/>. Acesso em: 01 set. 2014.2163-1646http://www.repositorio.ufop.br/handle/123456789/3831Some mechanisms have been proposed to explain the role of bradykinin on glucose homeostasis and some studies reported that the BDKRB2 +9/−9 polymorphism was associated to the transcriptional activity of the receptor. In this scenario, the main aim of this study was to evaluate the association of the BDKRB2 +9/−9 polymorphism with diabetes mellitus risk in the Brazilian general population. This study included 1,032 subjects of the general urban population. Anthropometrical, blood pressure, biochemical, and genotype analyses for the BDKRB2 +9/−9 bp insertion/deletion polymorphism were performed. Individuals carrying +9/+9 or +9/−9 genotypes had higher glucose values (84.5mg/dL versus 80.6mg/dL, resp.) and higher frequency of diabetes mellitus (7.6% versus 3.6%, resp.) compared to individuals carrying −9/−9, adjusting for age and gender. In addition, higher diabetes mellitus risk was associated to presence of the +9/+9 or +9/−9 genotypes (OR= 1.91; 95% CI = 1.09–4.19; P = 0.03). Our data suggest that the BDKRB2 +9/-9 polymorphismmay act as a geneticmodulator of glucose homeostasis. It was previously associated to insulin sensitivity, glucose uptake, and insulin secretion, and, in this study, data suggest that the polymorphism may increase susceptibility to chronic metabolic conditions such as diabetes in the Brazilian population.en-USArtigo publicado em periodicoThis is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Fonte: Experimental Diabetes Research <http://www.hindawi.com/journals/jdr/2012/480251/>. Acesso em: 01 set. 2014.http://dx.doi.org/10.1155/2012/480251