Variations in Rodent Models of Type 1 Diabetes: Islet Morphology. (13th May 2013)

• Record Type: Journal Article
• Authors: Novikova, Lesya; Smirnova, Irina V.; Rawal, Sonia; Dotson, Abby L.; Benedict, Stephen H.; Stehno-Bittel, Lisa
• Other Names: Cameron Norman Academic Editor.
• Is Part Of: Journal of diabetes research. Volume 2013(2013)
• Publication Date: 2013-05-13
• Subjects: Diabetes -- Periodicals; Diabetes -- Pathophysiology -- Periodicals; Diabetes -- Prevention -- Periodicals; Diabetes -- Etiology -- Periodicals; Diabetes -- Epidemiology -- Periodicals; Diabetes -- Pathogenesis -- Periodicals; 616.462005
• DOI: 10.1155/2013/965832
• Languages: English
• ISSNs: 2314-6745

Abstract

Abstract : 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.