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Experimental Diabetes Research
Volume 2008, Article ID 305403, 7 pages
Research Article

Phlorizin Prevents Glomerular Hyperfiltration but not Hypertrophy in Diabetic Rats

1Department of Physiology, Faculty of Medicine, Kuwait University, P.O. Box 24923, Safat 13110, Kuwait
2Department of Pathology, Faculty of Medicine, Kuwait University, P.O. Box 24923, Safat 13110, Kuwait

Received 27 March 2008; Accepted 9 July 2008

Academic Editor: Mark Cooper

Copyright © 2008 Slava Malatiali et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The relationships of renal and glomerular hypertrophies to development of hyperfiltration and proteinuria early in streptozotocin-induced diabetes were explored. Control, diabetic, phlorizin-treated controls, and diabetic male Fischer rats were used. Phlorizin (an -glucose cotransport inhibitor) was given at a dose sufficient to normalize blood glucose. Inulin clearance () and protein excretion rate (PER) were measured. For morphometry, kidney sections were stained with periodic acid Schiff. At one week, diabetes PER increased 2.8-folds (), increased 80% (). Kidney wet and dry weights increased 10%–12% (), and glomerular tuft area increased 9.3% (). Phlorizin prevented proteinuria, hyperfiltration, and kidney hypertrophy, but not glomerular hypertrophy. Thus, hyperfiltration, proteinuria, and whole kidney hypertrophy were related to hyperglycemia but not to glomerular growth. Diabetic glomerular hypertrophy constitutes an early event in the progression of glomerular pathology which occurs in the absence of mesangial expansion and persists even after changes in protein excretion and GFR are reversed through glycemic control.