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Publication

Reduction in Podocyte Density as a Pathologic Feature in Early Diabetic Nephropathy in Rodents: Prevention of by Lipoic Acid Treatment

Authors Brian Siu, Jharna Saha, William E. Smoyer, Kelli A. Sullivan, Frank C. Brosius III Submitted By Frank Brosius on 8/6/2003 Status Published Journal BMC nephrology [electronic resource] Year 2006 Date Published 4/1/2006 Volume : Pages 7 : 1 - 11 PubMed Reference 16539708 Abstract Background. A reduction in the number of renal glomerular podocytes has been documented in the kidneys of patients with diabetes mellitus. Additional studies have shown that podocyte injury occurs in diabetes in both animal models and humans, but no determination of podocyte number has been reported in diabetic animals. Methods. The number and density of podocytes in glomeruli from rats and mice with streptozotocin (STZ)-diabetes mellitus was determined at several time points based on detection of the glomerular podocyte specific antigens, WT1 and GLEPP1. The effect of insulin administration or treatment with the antioxidant, Ą-lipoic acid, on podocyte number was also assessed. Results. Experimental diabetes resulted in a rapid decline in podocyte numbers. A significant reduction in podocytes/glomerular cross-section was found in STZ diabetes in rats at 2 weeks (14%) 6 weeks (18%) and 8 weeks (34%) following STZ injection. Similar declines in podocyte number were found in STZ diabetes in c57Bl6 mice at 2 weeks, but not at 3 days after injection. Treatment with Ą-lipoic acid substantially reversed the reduction in podocyte number in diabetic rats but treatment with insulin had only a modest effect in preventing the decline in podocyte number. Conclusions. STZ diabetes results in reduction in the number of podocytes within 2 weeks after onset of hyperglycemia. Prevention of these effects with antioxidant therapy suggests that podocyte loss is due in part to increased levels of reactive oxygen species as well as hyperglycemia.

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Genes
Symbol Description Ptpro protein tyrosine phosphatase, receptor type, O Wt1 Wilms tumor homolog