TY - JOUR
T1 - Akt and PTEN
T2 - β-cell mass and pancreas plasticity
AU - Elghazi, Lynda
AU - Bernal-Mizrachi, Ernesto
N1 - 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.
PY - 2009/7
Y1 - 2009/7
N2 - 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.
AB - 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.
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U2 - 10.1016/j.tem.2009.03.002
DO - 10.1016/j.tem.2009.03.002
M3 - Review article
C2 - 19541499
AN - SCOPUS:67649233039
VL - 20
SP - 243
EP - 251
JO - Trends in Endocrinology and Metabolism
JF - Trends in Endocrinology and Metabolism
SN - 1043-2760
IS - 5
ER -