Lack of AKT in adipocytes causes severe lipodystrophy

Mol Metab. 2016 May 13;5(7):472-479. doi: 10.1016/j.molmet.2016.05.006. eCollection 2016 Jul.

Abstract

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.

Keywords: Akt; Insulin resistance; Insulin signaling; Lipodystrophy.