[HTML][HTML] Lack of AKT in adipocytes causes severe lipodystrophy

AL Shearin, BR Monks, P Seale, MJ Birnbaum - Molecular metabolism, 2016 - Elsevier
AL Shearin, BR Monks, P Seale, MJ Birnbaum
Molecular metabolism, 2016Elsevier
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 …
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.
Elsevier