Figure 10.
Immunofluorescent labelling of islet cells rodent and primate diabetes to demonstrate changes in islet architecture in hyperglycemia. Panels show cells immunofluorescently labelled for insulin, glucagon, and somatostatin and the merged signals. Hyperglycemic models: (A) Diabetic Goto-Kakizaki rat; (B) mouse model of diabetes exhibiting beta-cell specific deletion of the Krebs cycle enzyme fumarate hydratase (FH-/-); (C) mouse with impaired insulin secretion due to the expression of an activating KATP channel mutation (βV59M); (D) non-human primate with diabetes; (E) patient with recent-onset T1D; and (F) patient with T2D. In all of these hyperglycemic models, there are marked changes in islet morphology (for comparison see Figure 2 for structure in the absence of diabetes). There was reduced insulin-positive areas and increased proportion of glucagon-positive cells. A typical feature of animal models of diabetes is an increased infiltration of α-cells into the core of the islet. Little change in the expression pattern of somatostatin is apparent in most of the diabetic models. However, somatostatin-expressing cells are increased in βV59M mice and in the patient sample of T1D. Scale, 200 μm.