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

Lack of AKT in adipocytes causes severe lipodystrophy.

Author information

1
Institute for Diabetes, Obesity, and Metabolism, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA, USA.
2
Institute for Diabetes, Obesity, and Metabolism, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA, USA; Department of Cell and Developmental Biology, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA, USA.
3
Institute for Diabetes, Obesity, and Metabolism, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA, USA. Electronic address: birnbaum@mail.med.upenn.edu.

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

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