International Mammalian Genome Society

17th International Mouse Genome Conference

9-12 November 2003, Braunschweig, Germany

Plenary Presentations * Oral Presentations *
Poster Presentations: Behavioural Genetics and Genomics * Development and Stem Cells * Functional Genome Analysis * Mouse Models of Human Disease * Mouse System Biology Bioinformatics * Multigenic and Multifactorial Trait Analysis * Nutrition and Metabolic Disease * Phenotyping Methods Imaging * The Genetics and Genomics of Infectious Disease *
Verne Chapman Memorial Lecture * Table of Contents * Sponsor/Exhibitor List * Awards * Photographs

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POSTER 189 - INHIBITION OF DIABETIC NEPHROPHATHY BY AMINOGUANIDINE IN DB/DB MICE

Gao X
Nanjing University

Co-Authors: Lu Y
Institutions: Nanjing University

End-stage renal failure is one of the leading causes for diabetic related lethality. This study evaluated the effects of aminoguanidine (AG), an inhibitor of advanced glycation end products (AGEs), on treatment of mesangial expansion and glomerular basement membrane thickening in the db/db mice. The db/db mouse is a well-characterized animal model for diabetes. In this study, db/db mice of 4 weeks or 5 months old were randomized into a non-treatment diabetic group and AG treatment diabetic group, whereas age-matched heterozygous non-diabetic mice as control. AG was administered at a dose of 36mg/kg daily by intraperitoneal injection for 4 weeks or 5 months. For 4 weeks old diabetic mice, AGEs levels increased over the 20 week period in kidney cortex, and this increase was attenuated by AG treatment. The AG treatment group also showed an improvement of renal function indicated by retardation of N-acel-β-D-glucosaminidase (NAG) activitie and creatine level. Histological examination showed that AG treatment prevented mesangial expansion in db/db mice. Continuous AG therapy for 5 months was more effective than that of 4 weeks treatment. AG treatment, however, did not affect the thickening of glomerular basement, elevation of body weight and blood glucose in db/db mice. Our results suggest that AG could inhibit the AGEs formation and diabetic nephropathy in diabetic mice.