PURPOSE: Experimental galactosemia and diabetes are known to result in diabetic-like retinopathy in animals, but the mechanism by which the retinopathy develops remains unclear.
Defects of retinal metabolism that are common to galactosemia and diabetes are closely associated with the development of retinopathy and might play a role in the pathogenesis of the retinal disease.
METHODS: Effects of experimental galactosemia on retinal calcium-activated ATPase [(Ca,Mg)-ATPase], sodium-potassium ATPase [(Na,K)-ATPase], glutathione, ATP, and pertinent ions have been compared with the effects of experimental diabetes in rat and dog models of diabetic retinopathy.
RESULTS: Activities of (Ca,Mg)-ATPase and (Na,K)-ATPase were decreased as a result of either experimental galactosemia or diabetes in both the dog and the rat, and the decreases were accompanied by a diminution of reduced glutathione (GSH) in the retina. Ouabain-insensitive ATPase activity in the retina was not significantly reduced by diabetes or galactosemia, suggesting that the observed defects in (Ca,Mg)-ATPase and (Na,K)-ATPase activities were specific. The decrease of retinal GSH levels was associated with an elevated concentration of oxidized glutathione in diabetes but not in galactosemia. Retinal ATP and ion concentrations remained unaffected by experimental galactosemia or diabetes.
CONCLUSIONS: Comparison of two etiologically dissimilar models of diabetic retinopathy (diabetes and galactosemia) has revealed abnormalities of retinal metabolism that are shared by the two models. Further comparisons of retinal metabolism between these two models should reveal additional sequelae of hyperglycemia that are associated with, and that might play a role in, the development of diabetic retinopathy.
TS Kern, RA Kowluru and RL Engerman Department of Ophthalmology and Visual Science, University of Wisconsin- Madison 53706-1532.
Investigative Ophthalmology & Visual Science, Vol 35, 2962-2967, Copyright © 1994 by Association for Research in Vision and Ophthalmology
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