Abstract
Some 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 (84.5 mg/dL versus 80.6 mg/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 polymorphism may act as a genetic modulator 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.
Highlights
Bradykinin (BK) is a nonapeptide formed by the action of a serine protease called kallikrein
Differences in age, gender, race/color, Body mass index (BMI), obesity, abdominal circumference, SBP, diastolic blood pressure (DBP), hypertension, TG, and total cholesterol (TC) according to genotype groups were not observed (+9/+9 plus +9/−9 versus −9/−9)
The main finding of this study was that the BDKRB2 +9/−9 polymorphism is associated with fasting glucose values and with diabetes mellitus risk in the Brazilian population
Summary
Bradykinin (BK) is a nonapeptide formed by the action of a serine protease called kallikrein. The kallikrein produces kinins which are largely released into interstitial fluid, blood, and glandular tissue, in particular by the pancreas. Several studies have demonstrated the role of BK in the modulation of important physiological effects such as inflammation, vascular permeability, hypotension, edema, smooth muscle contraction, and glucose homeostasis, and most of these actions are mediated by the B2 receptor (B2R) [1, 2]. Studies have reported that BK enhances the tyrosine phosphorylation of IRS1 and improves the binding affinity of IRS1 with the P85 regulatory subunit of PI3K, which increases the translocation of GLUT4 to the plasma membrane [3]. The activation of endothelial nitric oxide synthase (eNOS) by BK results in improved blood flow thereby increasing glucose supply to peripheral tissues [4]
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