Promiscuous affairs of PKB/AKT isoforms in metabolism

Arch Physiol Biochem. 2011 May;117(2):70-7. doi: 10.3109/13813455.2010.539236. Epub 2011 Jan 10.

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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Adipocytes / metabolism
  • Animals
  • Energy Metabolism / physiology
  • Gene Expression / physiology
  • Glucose / metabolism*
  • Humans
  • Insulin / metabolism*
  • Insulin Resistance
  • Isoenzymes / genetics
  • Isoenzymes / metabolism*
  • Liver / metabolism
  • Mice
  • Mice, Knockout
  • Muscle, Skeletal / metabolism
  • Organ Specificity
  • Pancreas / metabolism
  • Proto-Oncogene Proteins c-akt / genetics
  • Proto-Oncogene Proteins c-akt / metabolism*
  • Rats
  • Receptor, Insulin / metabolism
  • Signal Transduction / physiology*

Substances

  • Insulin
  • Isoenzymes
  • Receptor, Insulin
  • Proto-Oncogene Proteins c-akt
  • Glucose