title: Lack of AKT in adipocytes causes severe lipodystrophy.
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.
authors.affiliation: Institute for Diabetes, Obesity, and Metabolism, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA, USA.
authors.forename: Abigail L
authors.initials: AL
authors.lastname: Shearin
authors.affiliation: Institute for Diabetes, Obesity, and Metabolism, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA, USA.
authors.forename: Bobby R
authors.initials: BR
authors.lastname: Monks
authors.affiliation: 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.
authors.forename: Patrick
authors.initials: P
authors.lastname: Seale
authors.affiliation: 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.
authors.forename: Morris J
authors.initials: MJ
authors.lastname: Birnbaum
keywords: Akt; Insulin resistance; Insulin signaling; Lipodystrophy