Promiscuous affairs of PKB/AKT isoforms in metabolism

Abstract

The protein kinase B (PKB) family encompasses three isoforms; PKBα (AKT1), PKBβ (AKT2) and PKBγ (AKT3). PKBα and PKBβ but not PKBγ, are prominently expressed in classical insulin-sensitive tissues like liver, muscle and fat. Transgenic mice deficient for PKBα, PKBβ or PKBγ have been analysed to study the roles of PKB isoforms in metabolic regulation. Until recently, only loss of PKBβ was reported to result in metabolic disorders, especially insulin resistance, in humans and mice. However, a new study has shown that PKBα-deficient mice can show enhanced glucose tolerance accompanied by improved β-cell function and higher insulin sensitivity in adipocytes. These findings prompted us to review the relevant literature on the regulation of glucose metabolism by PKB isoforms in liver, skeletal muscle, adipocytes and pancreas.

Keywords::

• PKB
• AKT
• redundancy
• metabolism
• glucose
• liver
• muscle
• fat
• pancreas

Acknowledgements

JJ was supported by the Novo Nordisk Research Foundation, MN by the Takeda Foundation, OT by the Gebert Rüf Stiftung (GRS-027/06), and SMS and OT by the Swiss SystemsX.ch initiative LiverX of the Competence Center for Systems Physiology and Metabolic Diseases. The FMI is part of the Novartis Research Foundation. JJ and MN are supported via participation in COST Action BM0602.

Declaration of interest

The authors report no conflicts of interest.