Growing new endocrine pancreas in situ
Type 1 diabetes mellitus is a major cause of endstage renal disease in young adults. Maintenance of normoglycemia in type 1 diabetics using exogenous insulin is difficult under the best of circumstances. Transplantation therapies are limited by the scarcity of human donor organs, rendering a priorit...
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Veröffentlicht in: | Clinical and experimental nephrology 2006-03, Vol.10 (1), p.1-7 |
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description | Type 1 diabetes mellitus is a major cause of endstage renal disease in young adults. Maintenance of normoglycemia in type 1 diabetics using exogenous insulin is difficult under the best of circumstances. Transplantation therapies are limited by the scarcity of human donor organs, rendering a priority the identification of an alternative source for replacing insulin-secreting cells. Embryonic pancreatic primordia transplanted into diabetic animal hosts undergo selective endocrine differentiation in situ and normalize glucose tolerance. Pancreatic primordia can be transplanted across isogeneic, allogeneic, and both concordant (rat-to-mouse) and highly disparate (pig-to-rodent) xenogeneic barriers. Successful transplantation of pancreatic primordia depends on obtaining them at defined windows during embryonic development within which the risk of teratogenicity is eliminated, growth potential is maximized, and immunogenicity is reduced. Here we review studies exploring the potential for pancreatic organogenesis post-transplantation of embryonic primordia as a therapy for type 1 diabetes. |
doi_str_mv | 10.1007/s10157-005-0393-4 |
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Maintenance of normoglycemia in type 1 diabetics using exogenous insulin is difficult under the best of circumstances. Transplantation therapies are limited by the scarcity of human donor organs, rendering a priority the identification of an alternative source for replacing insulin-secreting cells. Embryonic pancreatic primordia transplanted into diabetic animal hosts undergo selective endocrine differentiation in situ and normalize glucose tolerance. Pancreatic primordia can be transplanted across isogeneic, allogeneic, and both concordant (rat-to-mouse) and highly disparate (pig-to-rodent) xenogeneic barriers. Successful transplantation of pancreatic primordia depends on obtaining them at defined windows during embryonic development within which the risk of teratogenicity is eliminated, growth potential is maximized, and immunogenicity is reduced. 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Maintenance of normoglycemia in type 1 diabetics using exogenous insulin is difficult under the best of circumstances. Transplantation therapies are limited by the scarcity of human donor organs, rendering a priority the identification of an alternative source for replacing insulin-secreting cells. Embryonic pancreatic primordia transplanted into diabetic animal hosts undergo selective endocrine differentiation in situ and normalize glucose tolerance. Pancreatic primordia can be transplanted across isogeneic, allogeneic, and both concordant (rat-to-mouse) and highly disparate (pig-to-rodent) xenogeneic barriers. Successful transplantation of pancreatic primordia depends on obtaining them at defined windows during embryonic development within which the risk of teratogenicity is eliminated, growth potential is maximized, and immunogenicity is reduced. Here we review studies exploring the potential for pancreatic organogenesis post-transplantation of embryonic primordia as a therapy for type 1 diabetes.</description><subject>Animals</subject><subject>Cell Transplantation - methods</subject><subject>Diabetes Mellitus, Type 1 - physiopathology</subject><subject>Humans</subject><subject>Organogenesis</subject><subject>Pancreas - anatomy & histology</subject><subject>Pancreas - embryology</subject><subject>Pancreas - growth & development</subject><subject>Pancreas, Artificial</subject><subject>Tissue Engineering - methods</subject><issn>1342-1751</issn><issn>1437-7799</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNpFkEFLAzEQhYMotlZ_gBdZPHiLznSSzeYopVah4EXPYbtJZIvN1mSX4r83pQsehpnDe28eH2O3CI8IoJ4SAkrFASQH0sTFGZuiIMWV0vo83yTmHJXECbtKaQsAlZb6kk2wlEKgwil7WMXu0IavIrhD4YLtmtgGV-zr0ERXp6INRWr74Zpd-Po7uZtxz9jny_Jj8crX76u3xfOaNyR0z-vSSyuPXSgX8-S8qoQuqRIOddkA5dlINwcHgrSzWCu05KsSrddWIs3Y_Sl3H7ufwaXebLshhvzSzLFCQpI6i_AkamKXUnTe7GO7q-OvQTBHMOYExmQw5ljGiOy5G4OHzc7Zf8dIgv4AMz9bfw</recordid><startdate>200603</startdate><enddate>200603</enddate><creator>Hammerman, Marc R</creator><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QP</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope></search><sort><creationdate>200603</creationdate><title>Growing new endocrine pancreas in situ</title><author>Hammerman, Marc R</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c349t-a6f5d503933157f3ef78496384e196c036c0b5e20e0439ed1a71d3f861df9d513</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Animals</topic><topic>Cell Transplantation - 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subjects | Animals Cell Transplantation - methods Diabetes Mellitus, Type 1 - physiopathology Humans Organogenesis Pancreas - anatomy & histology Pancreas - embryology Pancreas - growth & development Pancreas, Artificial Tissue Engineering - methods |
title | Growing new endocrine pancreas in situ |
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