Type 1 diabetes (T1D) is an autoimmune disease, characterized by the complete loss of functioning [insulin-producing] islets in the pancreas. T1D is linked to the human leukocyte antigen sequence, but environmental factors are believed to trigger the immune response. The immune system destroys the insulin-producing β cells in the islet, resulting in dangerously high blood glucose levels (BGL). This project focuses on T1D's effect and progression in the pancreas. By analyzing the rate of insulitis, we aim to create a model to describe diabetes onset. Our previous data suggest two plausible progression models which were categorized as linear or sudden decline. In the linear decline model, functioning islets are lost gradually until complete onset of T1D. Onset is identified by high BGL for two consecutive weeks, indicating catastrophic islet loss. The sudden decline model is defined by the rapid loss of islet over a relatively short time span. Using immunohistochemistry, the pancreata of non-obese diabetic (NOD) mice genetically predisposed to T1D are embedded in paraffin, mounted on positive slides, and stained for insulin and glucagon. A metric system was created to categorize the islet loss severity over the 35-week period. The initial twelve weeks are analyzed here to determine if separate populations related to age of onset can be determined by the rate of immune cell infiltration. If two populations exist, early progressors to T1D will decline more rapidly. This analysis will allow for better characterization of T1D progression, which is still poorly understood despite its increasing prevalence.

Determining a progression timeline of type 1 diabetes through decreasing insulin production

2019 Spring National Meeting

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