Presence of residual beta cells and co-existing islet autoimmunity in the NOD mouse during longstanding diabetes: a combined histochemical and immunohistochemical study |
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Authors: | Shiva Reddy Ryan Chau Chia Chai Jessica Astrid Rodrigues Tzu-Hsuan Hsu Elizabeth Robinson |
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Institution: | (1) School of Biological Sciences, University of Auckland, Private Bag 92019, Auckland, New Zealand;(2) Department of Epidemiology and Biostatistics, School of Population Health, Faculty of Medical and Health Sciences, University of Auckland, Private Bag 92019, Auckland, New Zealand |
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Abstract: | During type 1 diabetes, most beta cells die by immune processes. However, the precise fate and characteristics of beta cells
and islet autoimmunity after onset are unclear. Here, the extent of beta cell survival was determined in the non-obese diabetic
(NOD) mouse during increasing duration of disease and correlated with insulitis. Pancreata from female NOD mice at diagnosis
and at 1, 2, 3 and 4 weeks thereafter were analysed immunohistochemically for insulin, glucagon and somatostatin cells and
glucose transporter-2 (glut2) and correlated with the degree of insulitis and islet immune cell phenotypes. Insulitis, although
variable, persisted after diabetes and declined with increasing duration of disease. During this period, beta cells also declined
sharply whereas glucagon and somatostatin cells increased, with occasional islet cells co-expressing insulin and glucagon.
Glut2 was absent in insulin-containing cells from 1 week onwards. CD4 and CD8 T cells and macrophages persisted until 4 weeks,
in islets with residual beta cells or extensive insulitis. We conclude that after diabetes onset, some beta cells survive
for extended periods, with continuing autoimmunity and expansion of glucagon and somatostatin cells. The absence of glut2
in several insulin-positive cells suggests that some beta cells may be unresponsive to glucose. |
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Keywords: | Beta cells NOD mouse Diabetes Insulitis Glucose transporter-2 |
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