Regulation of pancreatic -cell growth and survival by the serine/threonine protein kinase Akt1/PKB
Robyn L. Tuttle1, Navdeep S. Gill2, William Pugh4, Jean-Pyo Lee4, Brigitte Koeberlein3, Emma E. Furth2, Kenneth S. Polonsky4, Ali Naji3
& Morris J. Birnbaum1
1
Howard Hughes Medical Institute, Department of Internal Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA
2
Department of Pathology & Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA
3
Department of Surgery, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA
4
Department of Medicine, Washington University School of Medicine, St. Louis, Missouri, USA
The physiological performance of an organ depends on an interplay between changes in cellular function and organ size, determined by cell growth, proliferation and death. Nowhere is this more evident than in the endocrine pancreas, where disturbances in function or mass result in severe disease. Recently, the insulin signal-transduction pathway has been implicated in both the regulation of hormone secretion from cells in mammals as well as the determination of cell and organ size in Drosophila melanogaster. A prominent mediator of the actions of insulin and insulin-like growth factor 1 (IGF-1) is the 3'-phosphoinositide−dependent protein kinase Akt, also known as protein kinase B (PKB). Here we report that overexpression of active Akt1 in the mouse cell substantially affects compartment size and function. There was a significant increase in both -cell size and total islet mass, accompanied by improved glucose tolerance and complete resistance to experimental diabetes.
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-cell growth and survival by the serine/threonine protein kinase Akt1/PKB
cells in mammals as well as the determination of cell and organ size in Drosophila melanogaster. A prominent mediator of the actions of insulin and insulin-like growth factor 1 (IGF-1) is the 3'-phosphoinositide−dependent protein kinase Akt, also known as protein kinase B (PKB). Here we report that overexpression of active Akt1 in the mouse 
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