| First Author | Sales VM | Year | 2019 |
| Journal | Diabetes | Volume | 68 |
| Issue | 8 | Pages | 1614-1623 |
| PubMed ID | 31167880 | Mgi Jnum | J:277519 |
| Mgi Id | MGI:6331185 | Doi | 10.2337/db18-1150 |
| Citation | Sales VM, et al. (2019) Kinin B1 Receptor Acts in Adipose Tissue to Control Fat Distribution in a Cell-Nonautonomous Manner. Diabetes 68(8):1614-1623 |
| abstractText | 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. |
