Variations in Rodent Models of Type 1 Diabetes : Islet Morphology

Abstract EN

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.