Akt and PTEN: beta-cell mass and pancreas plasticity

Trends Endocrinol Metab. 2009 Jul;20(5):243-51. doi: 10.1016/j.tem.2009.03.002. Epub 2009 Jun 21.

Abstract

The capacity of pancreatic beta-cells to adapt to insulin resistance is crucial for glucose homeostasis and is a factor in the development of type 2 diabetes. The insulin receptor substrate (insulin receptor 2/phosphoinositide 3-kinase [PI3K]) pathway plays a crucial part in regulating beta-cell mass and function. The serine-threonine kinase Akt, also known as protein kinase B, is one of the major downstream targets of the PI3K pathway and is negatively regulated by phosphatase and tensin homologue deleted on chromosome 10. This Akt signaling pathway has recently been implicated in cell-cycle progression and survival of pancreatic beta-cells. Understanding the mechanisms that link Akt to modulation of beta-cell mass, function and plasticity will positively affect treatment of human diabetes.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Humans
  • Insulin-Secreting Cells / metabolism*
  • Insulin-Secreting Cells / physiology
  • Models, Biological
  • PTEN Phosphohydrolase / metabolism
  • PTEN Phosphohydrolase / physiology*
  • Pancreas / metabolism*
  • Pancreas / physiology
  • Proto-Oncogene Proteins c-akt / metabolism
  • Proto-Oncogene Proteins c-akt / physiology*
  • Signal Transduction / physiology

Substances

  • Proto-Oncogene Proteins c-akt
  • PTEN Phosphohydrolase