| First Author | Shearin AL | Year | 2016 |
| Journal | Mol Metab | Volume | 5 |
| Issue | 7 | Pages | 472-479 |
| PubMed ID | 27408773 | Mgi Jnum | J:294195 |
| Mgi Id | MGI:6453326 | Doi | 10.1016/j.molmet.2016.05.006 |
| Citation | Shearin AL, et al. (2016) Lack of AKT in adipocytes causes severe lipodystrophy. Mol Metab 5(7):472-479 |
| abstractText | OBJECTIVE: Adipose depot mass is tightly regulated to maintain energy homeostasis. AKT is a critical kinase in the insulin-signaling cascade that is required for the process of adipogenesis in vitro. However, the role of AKT in the maintenance and/or function of mature adipocytes in vivo had not been examined. METHODS: To study this, we deleted Akt1 and Akt2 in adipocytes of mice using the AdipoQ-Cre driver. RESULTS: Strikingly, mice lacking adipocyte AKT were severely lipodystrophic, having dramatically reduced gonadal adipose and no discernible subcutaneous or brown adipose tissue. As a result, these mice developed severe insulin resistance accompanied by fatty liver, hepatomegaly and with enlarged islets of Langerhans. CONCLUSIONS: These data reveal the critical role of adipocyte AKT and insulin signaling for maintaining adipose tissue mass. |
