Variations in Rodent Models of Type 1 Diabetes: Islet Morphology
Type 1 diabetes (T1D) is characterized by hyperglycemia due to lost or damaged islet insulin-producing β-cells. Rodent models of T1D result in hyperglycemia, but with different forms of islet deterioration. This study focused on 1 toxin-induced and 2 autoimmune rodent models of T1D: BioBreeding Diab...
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| Format: | Article |
| Language: | English |
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Wiley
2013-01-01
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| Series: | Journal of Diabetes Research |
| Online Access: | http://dx.doi.org/10.1155/2013/965832 |
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| author | Lesya Novikova Irina V. Smirnova Sonia Rawal Abby L. Dotson Stephen H. Benedict Lisa Stehno-Bittel |
| author_facet | Lesya Novikova Irina V. Smirnova Sonia Rawal Abby L. Dotson Stephen H. Benedict Lisa Stehno-Bittel |
| author_sort | Lesya Novikova |
| collection | DOAJ |
| description | Type 1 diabetes (T1D) is characterized by hyperglycemia due to lost or damaged islet insulin-producing β-cells. Rodent models of T1D result in hyperglycemia, but with different forms of islet deterioration. This study focused on 1 toxin-induced and 2 autoimmune rodent models of T1D: BioBreeding Diabetes Resistant rats, nonobese diabetic mice, and Dark Agouti rats treated with streptozotocin. Immunochemistry was used to evaluate the insulin levels in the β-cells, cell composition, and insulitis. T1D caused complete or significant loss of β-cells in all animal models, while increasing numbers of α-cells. Lymphocytic infiltration was noted in and around islets early in the progression of autoimmune diabetes. The loss of lymphocytic infiltration coincided with the absence of β-cells. In all models, the remaining α- and δ-cells regrouped by relocating to the islet center. The resulting islets were smaller in size and irregularly shaped. Insulin injections subsequent to induction of toxin-induced diabetes significantly preserved β-cells and islet morphology. Diabetes in animal models is anatomically heterogeneous and involves important changes in numbers and location of the remaining α- and δ-cells. Comparisons with human pancreatic sections from healthy and diabetic donors showed similar morphological changes to the diabetic BBDR rat model. |
| format | Article |
| id | doaj-art-9baefc3ed2fa479aa37decde7cccee89 |
| institution | Kabale University |
| issn | 2314-6745 2314-6753 |
| language | English |
| publishDate | 2013-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Journal of Diabetes Research |
| spelling | doaj-art-9baefc3ed2fa479aa37decde7cccee892025-02-03T01:26:05ZengWileyJournal of Diabetes Research2314-67452314-67532013-01-01201310.1155/2013/965832965832Variations in Rodent Models of Type 1 Diabetes: Islet MorphologyLesya Novikova0Irina V. Smirnova1Sonia Rawal2Abby L. Dotson3Stephen H. Benedict4Lisa Stehno-Bittel5Department of Physical Therapy and Rehabilitation Science, University of Kansas Medical Center, Kansas City, KS 66160, USADepartment of Physical Therapy and Rehabilitation Science, University of Kansas Medical Center, Kansas City, KS 66160, USADepartment of Physical Therapy and Rehabilitation Science, University of Kansas Medical Center, Kansas City, KS 66160, USADepartment of Molecular Biosciences, University of Kansas, Lawrence, KS 66045, USADepartment of Molecular Biosciences, University of Kansas, Lawrence, KS 66045, USADepartment of Physical Therapy and Rehabilitation Science, University of Kansas Medical Center, Kansas City, KS 66160, USAType 1 diabetes (T1D) is characterized by hyperglycemia due to lost or damaged islet insulin-producing β-cells. Rodent models of T1D result in hyperglycemia, but with different forms of islet deterioration. This study focused on 1 toxin-induced and 2 autoimmune rodent models of T1D: BioBreeding Diabetes Resistant rats, nonobese diabetic mice, and Dark Agouti rats treated with streptozotocin. Immunochemistry was used to evaluate the insulin levels in the β-cells, cell composition, and insulitis. T1D caused complete or significant loss of β-cells in all animal models, while increasing numbers of α-cells. Lymphocytic infiltration was noted in and around islets early in the progression of autoimmune diabetes. The loss of lymphocytic infiltration coincided with the absence of β-cells. In all models, the remaining α- and δ-cells regrouped by relocating to the islet center. The resulting islets were smaller in size and irregularly shaped. Insulin injections subsequent to induction of toxin-induced diabetes significantly preserved β-cells and islet morphology. Diabetes in animal models is anatomically heterogeneous and involves important changes in numbers and location of the remaining α- and δ-cells. Comparisons with human pancreatic sections from healthy and diabetic donors showed similar morphological changes to the diabetic BBDR rat model.http://dx.doi.org/10.1155/2013/965832 |
| spellingShingle | Lesya Novikova Irina V. Smirnova Sonia Rawal Abby L. Dotson Stephen H. Benedict Lisa Stehno-Bittel Variations in Rodent Models of Type 1 Diabetes: Islet Morphology Journal of Diabetes Research |
| title | Variations in Rodent Models of Type 1 Diabetes: Islet Morphology |
| title_full | Variations in Rodent Models of Type 1 Diabetes: Islet Morphology |
| title_fullStr | Variations in Rodent Models of Type 1 Diabetes: Islet Morphology |
| title_full_unstemmed | Variations in Rodent Models of Type 1 Diabetes: Islet Morphology |
| title_short | Variations in Rodent Models of Type 1 Diabetes: Islet Morphology |
| title_sort | variations in rodent models of type 1 diabetes islet morphology |
| url | http://dx.doi.org/10.1155/2013/965832 |
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