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Acta Physiologica 2012; Volume 206, Supplement 691
Scandinavian Physiological Society's Annual Meeting
8/24/2012-8/26/2012
Helsinki, Finland
SUSCEPTIBILITY TO DEVELOP DIABETIC NEPHROPATHY IN FOUR MOUSE MODELS OF TYPE-1 DIABETES.
Abstract number: F02
FRANZEN1 S, FASCHING1 A, HANSELL1 P, PALM1 F
1BOX 571, 75123 Uppsala: Sweden
Diabetic nephropathy (DN) develops in about 30% of all diabetics even though insulin is administered to control the blood glucose. Adequate experimental animal models are needed in order to further our understanding regarding the involved pathological mechanisms. Type 1 diabetic mouse models are frequently used since they resemble human DN. However, the most commonly used mouse strain, C57/Bl6, develop only minor kidney damage even after prolonged diabetes duration. We therefore investigated the susceptibility to develop DN in four commonly used mouse models, namely C57/Bl6, NMRI, Balb/c and 129Sv. Insulinopenic diabetes was induced (alloxan 6775 mg/kg) to achieve blood glucose above 15 mmol/l. Conscious glomerular filtration rate (GFR) was measured using the FITC-inulin bolus injection technique and proteinuria was measured using 24h urine collection in metabolic cages. All measurements were performed at baseline and after five and ten weeks after diabetes induction. GFR were significantly elevated in C57/Bl6, NMRI and 129Sv at the end of the study. NMRI had the largest increase in GFR and Balb/c did not develop glomerular hyperfiltration. NMRI and 129Sv displayed profound proteinuria, while C57/Bl6 and Balb/c did not. In conclusion, there are differences among these mouse strains regarding the response in GFR to sustained insulinopenic diabetes. Although the magnitude of proteinuria varied among the different mouse strains, oxidative stress may still affect renal function for example in terms of electrolyte handling. These findings should be considered when deciding on study designs of future investigations to elucidate the mechanisms involved in the development of DN.
To cite this abstract, please use the following information:
Acta Physiologica 2012; Volume 206, Supplement 691 :F02