Bdkrb1 participates in the pathogenesis of LIEP bone loss possibly through mechanisms that involve modulation of the TH 17 response, thereby demonstrating its role in the development of periodontitis.

The kinin B1 receptor (B1R) plays a role in inflammatory and metabolic processes. B1R deletion (B1−/−) protects mice from diet-induced obesity and improves insulin and leptin sensitivity. In contrast, genetic reconstitution of B1R exclusively in adipose tissue reverses the lean phenotype of B1−/− mice. To study the cell-nonautonomous nature of these effects, we transplanted epididymal white adipose tissue (eWAT) from wild-type donors (B1+/+) into B1−/− mice (B1+/+→B1−/−) and compared them with autologous controls (B1+/+→B1+/+ or B1−/−→B1−/−). We then fed these mice a high-fat diet for 16 weeks and investigated their metabolic phenotypes. B1+/+→B1−/− mice became obese but not glucose intolerant or insulin resistant, unlike B1−/−→B1−/− mice. Moreover, the endogenous adipose tissue of B1+/+→B1−/− mice exhibited higher expression of adipocyte markers (e.g., Fabp4 and Adipoq) and changes in the immune cell pool. These mice also developed fatty liver. Wild-type eWAT transplanted into B1−/− mice normalized circulating insulin, leptin, and epidermal growth factor levels. In conclusion, we demonstrated that B1R in adipose tissue controls the response to diet-induced obesity by promoting adipose tissue expansion and hepatic lipid accumulation in cell-nonautonomous manners.