To test whether treatment with aminoguanidine, a drug known to prevent cross-linking between glycated proteins, is effective in improving reduced erythrocyte deformability in diabetes, we studied a group (n = 6) of ALX-induced long-term (12.7 ± 2.2 mo of hyperglycemia) diabetic New Zealand white rabbits before and after 20 wk of treatment with aminoguanidine (100 mg.kg−1 · day−1). The key findings were as follows: 1) at 12 wk of treatment with aminoguanidine, mean erythrocyte deformability normalized and remained within the normal reference range throughout the period of aminoguanidine administration; 2) 10 wk after discontinuing aminoguanidine in a subset of diabetic rabbits, mean erythrocyte deformability deteriorated by ∼50%; 3) blood glucose and total GHb did not vary significantly during treatment with aminoguanidine nor after its discontinuation.
Correction of Erythrocyte Deformability Defect in ALX-Induced Diabetic Rabbits After Treatment With Aminoguanidine
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Clinton D Brown, Zhong H Zhao, Fernando De Alvaro, Seewai Chan, Eli A Friedman; Correction of Erythrocyte Deformability Defect in ALX-Induced Diabetic Rabbits After Treatment With Aminoguanidine. Diabetes 1 April 1993; 42 (4): 590–593. https://doi.org/10.2337/diab.42.4.590
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