B-cell death and mass in syngeneically transplanted islets exposed to short and long-term hyperglycemia
We studied the effects of hyperglycemia on beta-cell death and mass in syngeneically transplanted islets. Six groups of STZ-induced diabetic C57BL/6 mice were transplanted with 100 syngeneic islets, an insufficient beta-cell mass to restore normoglycemia. Groups 1, 2, and 3 remained hyperglycemic th...
| Autores: | , , , , , |
|---|---|
| Tipo de recurso: | artículo |
| Estado: | Versión publicada |
| Fecha de publicación: | 2002 |
| País: | España |
| Institución: | Universidad de Barcelona |
| Repositorio: | Dipòsit Digital de la UB |
| OAI Identifier: | oai:diposit.ub.edu:2445/135009 |
| Acceso en línea: | https://hdl.handle.net/2445/135009 |
| Access Level: | acceso abierto |
| Palabra clave: | Diabetis Cirurgia experimental Hiperglucèmia Illots de Langerhans Diabetes Experimental surgery Hyperglycemia Islands of Langerhans |
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B-cell death and mass in syngeneically transplanted islets exposed to short and long-term hyperglycemiaBiarnés Costa, MontseMontolio Rusiñol, MartaNacher, VictorRaurell, MercèSoler Ramon, JoanMontanya Mias, EduardDiabetisCirurgia experimentalHiperglucèmiaIllots de LangerhansDiabetesExperimental surgeryHyperglycemiaIslands of LangerhansWe studied the effects of hyperglycemia on beta-cell death and mass in syngeneically transplanted islets. Six groups of STZ-induced diabetic C57BL/6 mice were transplanted with 100 syngeneic islets, an insufficient beta-cell mass to restore normoglycemia. Groups 1, 2, and 3 remained hyperglycemic throughout the study. Groups 4, 5, and 6 were treated with insulin from day 7 before transplantation to day 10 after transplantation. After insulin discontinuation, group 6 mice achieved definitive normoglycemia. Grafts were harvested at 3 (groups 1 and 4), 10 (groups 2 and 5), and 30 (groups 3 and 6) days after transplantation. On day 3, the initially transplanted beta-cell mass (0.13 +/- 0.01 mg) was dramatically and similarly reduced in the hyperglycemic and insulin-treated groups (group 1: 0.048 +/- 0.002 mg; group 4: 0.046 +/- 0.007 mg; P < 0.001). Extensive islet necrosis (group 1: 30.7%; group 4: 26.8%) and increased beta-cell apoptosis (group 1: 0.30 +/- 0.05%; group 4: 0.42 +/- 0.07%) were found. On day 10, apoptosis remained increased in both hyperglycemic and insulin-treated mice (group 2: 0.44 +/- 0.09%; group 5: 0.48 +/- 0.08%) compared with normal pancreas (0.04 +/- 0.03%; P < 0.001). In contrast, on day 30, beta-cell apoptosis was increased in grafts exposed to sustained hyperglycemia (group 3: 0.37 +/- 0.03%) but not in normoglycemic mice (group 6: 0.12 +/- 0.02%); beta-cell mass was selectively reduced in islets exposed to hyperglycemia (group 3: 0.046 +/- 0.02 mg; group 6: 0.102 +/- 0.009 mg; P < 0.01). In summary, even in optimal conditions, approximately 60% of transplanted islet tissue was lost 3 days after syngeneic transplantation, and both apoptosis and necrosis contributed to beta-cell death. Increased apoptosis and reduced beta-cell mass were also found in islets exposed to chronic hyperglycemia, suggesting that sustained hyperglycemia increased apoptosis in transplanted beta-cells.American Diabetes Association2002info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdfhttps://hdl.handle.net/2445/135009Articles publicats en revistes (Ciències Clíniques)reponame:Dipòsit Digital de la UBinstname:Universidad de BarcelonaInglésReproducció del document publicat a: https://doi.org/10.2337/diabetes.51.1.66Diabetes, 2002, vol. 51, num. 1, p. 66-72https://doi.org/10.2337/diabetes.51.1.66cc-by-nc-nd (c) American Diabetes Association, 2002http://creativecommons.org/licenses/by-nc-nd/3.0/esinfo:eu-repo/semantics/openAccessoai:diposit.ub.edu:2445/1350092026-05-27T06:46:51Z |
| dc.title.none.fl_str_mv |
B-cell death and mass in syngeneically transplanted islets exposed to short and long-term hyperglycemia |
| title |
B-cell death and mass in syngeneically transplanted islets exposed to short and long-term hyperglycemia |
| spellingShingle |
B-cell death and mass in syngeneically transplanted islets exposed to short and long-term hyperglycemia Biarnés Costa, Montse Diabetis Cirurgia experimental Hiperglucèmia Illots de Langerhans Diabetes Experimental surgery Hyperglycemia Islands of Langerhans |
| title_short |
B-cell death and mass in syngeneically transplanted islets exposed to short and long-term hyperglycemia |
| title_full |
B-cell death and mass in syngeneically transplanted islets exposed to short and long-term hyperglycemia |
| title_fullStr |
B-cell death and mass in syngeneically transplanted islets exposed to short and long-term hyperglycemia |
| title_full_unstemmed |
B-cell death and mass in syngeneically transplanted islets exposed to short and long-term hyperglycemia |
| title_sort |
B-cell death and mass in syngeneically transplanted islets exposed to short and long-term hyperglycemia |
| dc.creator.none.fl_str_mv |
Biarnés Costa, Montse Montolio Rusiñol, Marta Nacher, Victor Raurell, Mercè Soler Ramon, Joan Montanya Mias, Eduard |
| author |
Biarnés Costa, Montse |
| author_facet |
Biarnés Costa, Montse Montolio Rusiñol, Marta Nacher, Victor Raurell, Mercè Soler Ramon, Joan Montanya Mias, Eduard |
| author_role |
author |
| author2 |
Montolio Rusiñol, Marta Nacher, Victor Raurell, Mercè Soler Ramon, Joan Montanya Mias, Eduard |
| author2_role |
author author author author author |
| dc.subject.none.fl_str_mv |
Diabetis Cirurgia experimental Hiperglucèmia Illots de Langerhans Diabetes Experimental surgery Hyperglycemia Islands of Langerhans |
| topic |
Diabetis Cirurgia experimental Hiperglucèmia Illots de Langerhans Diabetes Experimental surgery Hyperglycemia Islands of Langerhans |
| description |
We studied the effects of hyperglycemia on beta-cell death and mass in syngeneically transplanted islets. Six groups of STZ-induced diabetic C57BL/6 mice were transplanted with 100 syngeneic islets, an insufficient beta-cell mass to restore normoglycemia. Groups 1, 2, and 3 remained hyperglycemic throughout the study. Groups 4, 5, and 6 were treated with insulin from day 7 before transplantation to day 10 after transplantation. After insulin discontinuation, group 6 mice achieved definitive normoglycemia. Grafts were harvested at 3 (groups 1 and 4), 10 (groups 2 and 5), and 30 (groups 3 and 6) days after transplantation. On day 3, the initially transplanted beta-cell mass (0.13 +/- 0.01 mg) was dramatically and similarly reduced in the hyperglycemic and insulin-treated groups (group 1: 0.048 +/- 0.002 mg; group 4: 0.046 +/- 0.007 mg; P < 0.001). Extensive islet necrosis (group 1: 30.7%; group 4: 26.8%) and increased beta-cell apoptosis (group 1: 0.30 +/- 0.05%; group 4: 0.42 +/- 0.07%) were found. On day 10, apoptosis remained increased in both hyperglycemic and insulin-treated mice (group 2: 0.44 +/- 0.09%; group 5: 0.48 +/- 0.08%) compared with normal pancreas (0.04 +/- 0.03%; P < 0.001). In contrast, on day 30, beta-cell apoptosis was increased in grafts exposed to sustained hyperglycemia (group 3: 0.37 +/- 0.03%) but not in normoglycemic mice (group 6: 0.12 +/- 0.02%); beta-cell mass was selectively reduced in islets exposed to hyperglycemia (group 3: 0.046 +/- 0.02 mg; group 6: 0.102 +/- 0.009 mg; P < 0.01). In summary, even in optimal conditions, approximately 60% of transplanted islet tissue was lost 3 days after syngeneic transplantation, and both apoptosis and necrosis contributed to beta-cell death. Increased apoptosis and reduced beta-cell mass were also found in islets exposed to chronic hyperglycemia, suggesting that sustained hyperglycemia increased apoptosis in transplanted beta-cells. |
| publishDate |
2002 |
| dc.date.none.fl_str_mv |
2002 |
| dc.type.none.fl_str_mv |
info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion |
| format |
article |
| status_str |
publishedVersion |
| dc.identifier.none.fl_str_mv |
https://hdl.handle.net/2445/135009 |
| url |
https://hdl.handle.net/2445/135009 |
| dc.language.none.fl_str_mv |
Inglés |
| language_invalid_str_mv |
Inglés |
| dc.relation.none.fl_str_mv |
Reproducció del document publicat a: https://doi.org/10.2337/diabetes.51.1.66 Diabetes, 2002, vol. 51, num. 1, p. 66-72 https://doi.org/10.2337/diabetes.51.1.66 |
| dc.rights.none.fl_str_mv |
cc-by-nc-nd (c) American Diabetes Association, 2002 http://creativecommons.org/licenses/by-nc-nd/3.0/es info:eu-repo/semantics/openAccess |
| rights_invalid_str_mv |
cc-by-nc-nd (c) American Diabetes Association, 2002 http://creativecommons.org/licenses/by-nc-nd/3.0/es |
| eu_rights_str_mv |
openAccess |
| dc.format.none.fl_str_mv |
application/pdf |
| dc.publisher.none.fl_str_mv |
American Diabetes Association |
| publisher.none.fl_str_mv |
American Diabetes Association |
| dc.source.none.fl_str_mv |
Articles publicats en revistes (Ciències Clíniques) reponame:Dipòsit Digital de la UB instname:Universidad de Barcelona |
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Universidad de Barcelona |
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Dipòsit Digital de la UB |
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Dipòsit Digital de la UB |
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1869420517787697152 |
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