Animal Models in Diabetes Research by Hans-Georg Joost, Hadi Al-Hasani, Annette Schürmann

By Hans-Georg Joost, Hadi Al-Hasani, Annette Schürmann

Detailing the newest protocols for getting to know animal types of diabetes, particularly resistant teams of rodents comparable to the NOD mouse, and together with professional suggestion on implementation, it is a invaluable new quantity within the equipment in Molecular Biology sequence.

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B. Gurley suggesting that expression of B1R may have beneficial effects in DN in the absence of constitutively expressed B2R. These results demonstrate the critical role of the bradykinin system in protecting kidney from damage caused by diabetes mellitus, and provide a clear example in how the Akita model can be used effectively to study the pathomechanisms of diabetic kidney injury in mice. 2. Endothelial Nitric Oxide Synthase Deficiency in Akita Mice Endothelial dysfunction and damage are prevalent in patients with diabetes mellitus and contribute to the development of DN (25).

Data derived from studies on many different rat strains indicate that at least one class II RT1 B/Du allele is required for diabetes onset (2, 3). Mitogen-activated spleen cells from diabetic BBDP rats can transfer disease to MHC-compatible naïve recipients, confirming that the diabetes is autoimmune mediated (4). The most striking phenotype in all BBDP rats is a profound T cell lymphopenia which results from the spontaneous apoptosis of peripheral T cells soon after their emigration from the thymus (5–7).

1. Pathogenesis of Pancreatic Islets Diabetes in BBDP rats typically develops between 50 and 90 days of age, with both sexes having a similar frequency of occurrence (1). Although increased neonatal beta cell apoptosis has been suggested to play a role in diabetes susceptibility in the BB rat (and non-obese diabetic (NOD) mouse) (18), the first histomorphological change detectable in the BBDP pancreas is the infiltration of immune cells in the islets of Langerhans (insulitis). In this regard, the morphology of insulitis observed in humans is more similar to the BB rat than to that of the NOD mouse.

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