By Hans-Georg Joost, Hadi Al-Hasani, Annette Schürmann
Detailing the most recent protocols for getting to know animal versions of diabetes, specifically resistant teams of rodents reminiscent of the NOD mouse, and together with professional suggestion on implementation, it is a helpful new quantity within the tools in Molecular Biology sequence.
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Extra info for Animal Models in Diabetes Research
In a separate set of experiments, we determined the functional and structural characteristics of kidney disease in FVB/NJ Akita mice. In this study, male FVB/NJ Akita mice developed sustained hyperglycemia and albuminuria by 4 and 8 weeks of age, respectively. By 20 weeks of age, diabetic animals developed a tenfold increase in albuminuria (480 ± 73 mg/day (Akita) vs. 0001) as well as renal and glomerular hypertrophy. Levels of albuminuria in FVB/NJ Akita mice suggest a moderate to severe susceptibility to renal injury resulting from type 1 diabetes, with 24-h urinary albumin excretion values being greater than the strains reported by Gurley and coworkers (8, 9).
Ramanathan S, Poussier P (2001) BB rat lyp mutation and type 1 diabetes. Immunol Rev 184:161–171 7. Yale JF, Grose M, Marliss EB (1985) Time course of the lymphopenia in BB rats. Relation to the onset of diabetes. Diabetes 34:955–959 8. Awata T, Guberski DL, Like AA (1995) Genetics of the BB rat: association of autoimmune disorders (diabetes, insulitis, and thyroiditis) with lymphopenia and major histocompatibility complex class II. Endocrinology 136:5731–5735 9. Shin JH, Janer M, McNeney B et al (2007) IA-2 autoantibodies in incident type I diabetes patients are associated with a polyadenylation signal polymorphism in GIMAP5.
Clinical data show that diabetes onset is often preceded by exposure to a pathogen or other environmental factors. Although the exact identity of these environmental perturbants remains obscure, suggested candidates have included toxins, certain dietary components, and vaccination, but data to support these is not conclusive (50–53). To date, the strongest epidemiologic evidence for an environmental association with T1D is provided by virus exposure (54–56). Clinical data reveal that diabetes onset is often preceded by exposure to viral infections including mumps, rubella, rotavirus, parvovirus, and enteroviruses (57).
Animal Models in Diabetes Research by Hans-Georg Joost, Hadi Al-Hasani, Annette Schürmann