| First Author | Pydi SP | Year | 2019 |
| Journal | Nat Commun | Volume | 10 |
| Issue | 1 | Pages | 2936 |
| PubMed ID | 31270323 | Mgi Jnum | J:289324 |
| Mgi Id | MGI:6435000 | Doi | 10.1038/s41467-019-11003-4 |
| Citation | Pydi SP, et al. (2019) Adipocyte beta-arrestin-2 is essential for maintaining whole body glucose and energy homeostasis. Nat Commun 10(1):2936 |
| abstractText | beta-Arrestins are major regulators of G protein-coupled receptor-mediated signaling processes. Their potential roles in regulating adipocyte function in vivo remain unexplored. Here we report the novel finding that mice lacking beta-arrestin-2 (barr2) selectively in adipocytes show significantly reduced adiposity and striking metabolic improvements when consuming excess calories. We demonstrate that these beneficial metabolic effects are due to enhanced signaling through adipocyte beta3-adrenergic receptors (beta3-ARs), indicating that barr2 represents a potent negative regulator of adipocyte beta3-AR activity in vivo. Interestingly, essentially all beneficial metabolic effects caused by adipocyte barr2 deficiency are absent in adipocyte barr2-PRDM16 double KO mice, indicating that the metabolic improvements caused by the lack of barr2 in adipocytes are mediated by the browning/beiging of white adipose tissue. Our data support the novel concept that 'G protein-biased' beta3-AR agonists that do not promote beta3-AR/barr2 interactions may prove useful for the treatment of obesity and related metabolic disorders. |
