Akt and PTEN: β-cell mass and pancreas plasticity

Lynda Elghazi; Ernesto Bernal-Mizrachi

doi:10.1016/j.tem.2009.03.002

Akt and PTEN: β-cell mass and pancreas plasticity

Lynda Elghazi, Ernesto Bernal-Mizrachi

Medicine

Research output: Contribution to journal › Review article › peer-review

58 Scopus citations

Abstract

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 language	English (US)
Pages (from-to)	243-251
Number of pages	9
Journal	Trends in Endocrinology and Metabolism
Volume	20
Issue number	5
DOIs	https://doi.org/10.1016/j.tem.2009.03.002
State	Published - Jul 2009

ASJC Scopus subject areas

Endocrinology, Diabetes and Metabolism
Endocrinology

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title = "Akt and PTEN: β-cell mass and pancreas plasticity",

abstract = "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.",

author = "Lynda Elghazi and Ernesto Bernal-Mizrachi",

note = "Funding Information: This work was supported by grants from the National Institute of Health (R03 DK068028–01) and a Research Grant from the Juvenile Research Foundation. E.B-M. is a recipient of a Career Development Award from the American Diabetes Association. We apologize to those whose work has not been covered and cited because of space constraints. ",

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