In a rat model of insulin resistance induced by high glucose feeding, B1R increased the production of O2•- via the activation of NADPH oxidase while B1R antagonism prevented the enhanced basal production of O2•- by NADPH oxidase and the upregulation of inducible nitric oxide synthase (iNOS) in the aorta (Dias et al., 2010; Dias and Couture, 2012b). Here, BDKRB1 is linked to Insulin resistance.