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Reduction in Podocyte Density as a Pathologic Feature in Early Diabetic
Nephropathy in Rodents: Prevention of by Lipoic Acid Treatment
Brian Siu, Jharna Saha, William E. Smoyer, Kelli A. Sullivan, Frank C. Brosius
Frank Brosius on 8/6/2003
BMC nephrology [electronic resource]
Volume : Pages
7 : 1 - 11
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,
ƒÑ-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
ƒÑ-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.
Neuropathy & Neurocognition
protein tyrosine phosphatase, receptor type, O
Wilms tumor homolog
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Please acknowledge all posters, manuscripts or scientific materials that were generated in part or whole using funds from the Diabetic Complications Consortium(DiaComp) using the following text:
Financial support for this work provided by the NIDDK Diabetic Complications Consortium (RRID:SCR_001415, www.diacomp.org), grants DK076169 and DK115255
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