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Special Articles |
Division of Endocrinology and Metabolism, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15213
Address correspondence and requests for reprints to: Andrew F. Stewart, M.D., Chief, Endocrinology, University of Pittsburgh School of Medicine, BST E-1140, 3550 Terrace Street, Pittsburgh, Pennsylvania 15213. E-mail: stewart{at}msx.dept-med.pitt.edu * Supported by NIH
This is a particularly exciting time in the field of pancreatic islet growth, development, and survival. The recent publication of a study demonstrating that human pancreatic islet transplantation is both technically and immunologically feasible has highlighted the need for large supplies of pancreatic islets or pancreatic ß cells for larger-scale islet transplantation in patients with diabetes. This, together with a rapid expansion in the past several years of the understanding of mechanisms of islet growth, development, and survival, has accelerated and invigorated efforts to therapeutically harness the cellular mechanisms responsible for pancreatic ß-cell proliferation, survival, and development and to take advantage of this new knowledge to enhance the availability, survival, and function of pancreatic ß cells in human islet transplantation for diabetes mellitus. Here, we briefly review the confluence of events that have provided optimism and energy to the islet transplant field, and we focus on peptide growth factors that eventually may be deployed in the effort to augment islet mass and function in patients with diabetes.
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R. C. Vasavada, I. Cozar-Castellano, D. Sipula, and A. F. Stewart Tissue-Specific Deletion of the Retinoblastoma Protein in the Pancreatic {beta}-Cell Has Limited Effects on {beta}-Cell Replication, Mass, and Function Diabetes, January 1, 2007; 56(1): 57 - 64. [Abstract] [Full Text] [PDF] |
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Y. Lu, A. Ponton, H. Okamoto, S. Takasawa, P. L. Herrera, and J.-L. Liu Activation of the Reg family genes by pancreatic-specific IGF-I gene deficiency and after streptozotocin-induced diabetes in mouse pancreas Am J Physiol Endocrinol Metab, July 1, 2006; 291(1): E50 - E58. [Abstract] [Full Text] [PDF] |
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I. Cozar-Castellano, N. Fiaschi-Taesch, T. A. Bigatel, K. K. Takane, A. Garcia-Ocana, R. Vasavada, and A. F. Stewart Molecular Control of Cell Cycle Progression in the Pancreatic {beta}-Cell Endocr. Rev., June 1, 2006; 27(4): 356 - 370. [Abstract] [Full Text] [PDF] |
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L. Bouwens and I. Rooman Regulation of Pancreatic Beta-Cell Mass Physiol Rev, October 1, 2005; 85(4): 1255 - 1270. [Abstract] [Full Text] [PDF] |
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C. Dai, C.-G. Huh, S. S. Thorgeirsson, and Y. Liu {beta}-Cell-Specific Ablation of the Hepatocyte Growth Factor Receptor Results in Reduced Islet Size, Impaired Insulin Secretion, and Glucose Intolerance Am. J. Pathol., August 1, 2005; 167(2): 429 - 436. [Abstract] [Full Text] [PDF] |
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J. Roccisana, V. Reddy, R. C. Vasavada, J. A. Gonzalez-Pertusa, M. A. Magnuson, and A. Garcia-Ocana Targeted Inactivation of Hepatocyte Growth Factor Receptor c-met in {beta}-Cells Leads to Defective Insulin Secretion and GLUT-2 Downregulation Without Alteration of {beta}-Cell Mass Diabetes, July 1, 2005; 54(7): 2090 - 2102. [Abstract] [Full Text] [PDF] |
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X. Zhang, J. P. Gaspard, Y. Mizukami, J. Li, F. Graeme-Cook, and D. C. Chung Overexpression of Cyclin D1 in Pancreatic {beta}-Cells In Vivo Results in Islet Hyperplasia Without Hypoglycemia Diabetes, March 1, 2005; 54(3): 712 - 719. [Abstract] [Full Text] [PDF] |
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T. Brun, I. Franklin, L. St-Onge, A. Biason-Lauber, E. J. Schoenle, C. B. Wollheim, and B. R. Gauthier The diabetes-linked transcription factor PAX4 promotes {beta}-cell proliferation and survival in rat and human islets J. Cell Biol., December 20, 2004; 167(6): 1123 - 1135. [Abstract] [Full Text] [PDF] |
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Y. Lu, P. L. Herrera, Y. Guo, D. Sun, Z. Tang, D. LeRoith, and J.-L. Liu Pancreatic-Specific Inactivation of IGF-I Gene Causes Enlarged Pancreatic Islets and Significant Resistance to Diabetes Diabetes, December 1, 2004; 53(12): 3131 - 3141. [Abstract] [Full Text] [PDF] |
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I. Cozar-Castellano, K. K. Takane, R. Bottino, A.N. Balamurugan, and A. F. Stewart Induction of {beta}-Cell Proliferation and Retinoblastoma Protein Phosphorylation in Rat and Human Islets Using Adenovirus-Mediated Transfer of Cyclin-Dependent Kinase-4 and Cyclin D1 Diabetes, January 1, 2004; 53(1): 149 - 159. [Abstract] [Full Text] [PDF] |
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D. J. Drucker Glucagon-Like Peptide-1 and the Islet {beta}-Cell: Augmentation of Cell Proliferation and Inhibition of Apoptosis Endocrinology, December 1, 2003; 144(12): 5145 - 5148. [Full Text] [PDF] |
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L. Farilla, A. Bulotta, B. Hirshberg, S. Li Calzi, N. Khoury, H. Noushmehr, C. Bertolotto, U. Di Mario, D. M. Harlan, and R. Perfetti Glucagon-Like Peptide 1 Inhibits Cell Apoptosis and Improves Glucose Responsiveness of Freshly Isolated Human Islets Endocrinology, December 1, 2003; 144(12): 5149 - 5158. [Abstract] [Full Text] [PDF] |
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B. Zhang, M. Hosaka, Y. Sawada, S. Torii, S. Mizutani, M. Ogata, T. Izumi, and T. Takeuchi Parathyroid Hormone-Related Protein Induces Insulin Expression Through Activation of MAP Kinase-Specific Phosphatase-1 That Dephosphorylates c-Jun NH2-Terminal Kinase in Pancreatic {beta}-Cells Diabetes, November 1, 2003; 52(11): 2720 - 2730. [Abstract] [Full Text] [PDF] |
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C. Dai, Y. Li, J. Yang, and Y. Liu Hepatocyte Growth Factor Preserves Beta Cell Mass and Mitigates Hyperglycemia in Streptozotocin-induced Diabetic Mice J. Biol. Chem., July 11, 2003; 278(29): 27080 - 27087. [Abstract] [Full Text] [PDF] |
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H. Hui, A. Nourparvar, X. Zhao, and R. Perfetti Glucagon-Like Peptide-1 Inhibits Apoptosis of Insulin-Secreting Cells via a Cyclic 5'-Adenosine Monophosphate-Dependent Protein Kinase A- and a Phosphatidylinositol 3-Kinase-Dependent Pathway Endocrinology, April 1, 2003; 144(4): 1444 - 1455. [Abstract] [Full Text] [PDF] |
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Z. Wang, E. Moro, K. Kovacs, R. Yu, and S. Melmed Pituitary tumor transforming gene-null male mice exhibit impaired pancreatic beta cell proliferation and diabetes PNAS, March 18, 2003; 100(6): 3428 - 3432. [Abstract] [Full Text] [PDF] |
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M. Freemark, I. Avril, D. Fleenor, P. Driscoll, A. Petro, E. Opara, W. Kendall, J. Oden, S. Bridges, N. Binart, et al. Targeted Deletion of the PRL Receptor: Effects on Islet Development, Insulin Production, and Glucose Tolerance Endocrinology, April 1, 2002; 143(4): 1378 - 1385. [Abstract] [Full Text] [PDF] |
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A. Garcia-Ocana, R. C. Vasavada, A. Cebrian, V. Reddy, K. K. Takane, J.-C. Lopez-Talavera, and A. F. Stewart Transgenic Overexpression of Hepatocyte Growth Factor in the {beta}-Cell Markedly Improves Islet Function and Islet Transplant Outcomes in Mice Diabetes, December 1, 2001; 50(12): 2752 - 2762. [Abstract] [Full Text] [PDF] |
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