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
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
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.


Ptproprotein tyrosine phosphatase, receptor type, O
Wt1Wilms tumor homolog