Akt and PTEN: β-cell mass and pancreas plasticity

Research output: Contribution to journalReview articlepeer-review

64 Scopus citations


The capacity of pancreatic β-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 β-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 β-cells. Understanding the mechanisms that link Akt to modulation of β-cell mass, function and plasticity will positively affect treatment of human diabetes.

Original languageEnglish (US)
Pages (from-to)243-251
Number of pages9
JournalTrends in Endocrinology and Metabolism
Issue number5
StatePublished - Jul 2009
Externally publishedYes

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology


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