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

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

Detailing the most recent protocols for studying animal versions of diabetes, particularly resistant teams of rodents reminiscent of the NOD mouse, and together with professional recommendation on implementation, this can be a priceless new quantity within the tools in Molecular Biology sequence.

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Finally, Akita mice are commercially available, and the Ins2+/C96Y mutation can be easily intercrossed on other transgenic mouse lines to facilitate model development. As described in this chapter, these features of the Akita model may provide an ideal experimental platform for studying the mechanisms of diabetic kidney injury that exist in humans, and ultimately advance our progress toward a treatment for DN. 2 Diabetic Kidney Injury in Akita Mice 25 2. 1. 24-Hour Urine Collection for Mice (see Fig.

Because KRV is a rat specific parvovirus, it does not infect humans. The only significant parvovirus currently identified in humans is B19. Although there is little information on a possible association between human parvovirus B19 and T1D (85), a single case has been reported (86). Despite the viral specificity, the BBDR rat model is a valuable animal model for the study of virus-induced human T1D. Unlike some mouse models, KRV virus does not infect pancreatic cells directly, but induces autoimmune diabetes through alteration of the immune system.

Diabetes 54:2628–2637 14. Kakoki M, Smithies O (2009) The kallikreinkinin system in health and in diseases of the kidney. Kidney Int 75:1019–1030 15. Kakoki M et al (2010) Lack of both bradykinin B1 and B2 receptors enhances nephropathy, neuropathy, and bone mineral loss in Akita diabetic mice. Proc Natl Acad Sci U S A 107:10190–10195 16. Kakoki M et al (2004) Diabetic nephropathy is markedly enhanced in mice lacking the bradykinin B2 receptor. Proc Natl Acad Sci U S A 101:13302–13305 17. Rigat B et al (1990) An insertion/deletion polymorphism in the angiotensin I-converting enzyme gene accounting for half the variance of serum enzyme levels.

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