Promiscuous affairs of PKB/AKT isoforms in metabolism

Simon M. Schultze, Jørgen Jensen, Brian A. Hemmings, Oliver Tschopp, Markus Niessen
2011 Archives of Physiology and Biochemistry  
The protein kinase B (PKB) family encompasses three isoforms; PKB (AKT1), PKB (AKT2) and PKB (AKT3). PKB and PKB but not PKB, are prominently expressed in classical insulin-sensitive tissues like liver, muscle and fat. Transgenic mice deficient for PKB, PKB or PKB have been analysed to study the roles of PKB isoforms in metabolic regulation. Until recently, only loss of PKB was reported to result in metabolic disorders, especially insulin resistance, in humans and mice. However, a new study has
more » ... er, a new study has shown that PKB-deficient mice can show enhanced glucose tolerance accompanied by improved -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. Abstract The protein kinase B (PKB) family encompasses three isoforms; PKB (AKT1), PKB (AKT2) and PKB (AKT3). PKB and PKBbut not PKB, are prominently expressed in classical insulin-sensitive tissues like liver, muscle and fat. Transgenic mice deficient for PKB, PKB or PKB have been analysed to study the roles of PKB isoforms in metabolic regulation. Until recently, only loss of PKB was reported to result in metabolic disorders, especially insulin resistance, in humans and mice. However, a new study has shown that PKB-deficient mice show enhanced glucose tolerance accompanied by improved -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.
doi:10.3109/13813455.2010.539236 pmid:21214427 fatcat:txi7ulrk75dylljrx2dkxadnji