Retinal metabolic abnormalities in diabetic mouse: Comparison with diabetic rat

Purpose. Dogs and rats are commonly used to examine the pathogenesis of diabetic retinopathy, but mouse is sparingly studied as an animal model of diabetic retinopathy. In this study metabolic abnormalities, postulated to contribute to the development of retinopathy in diabetes, are investigated in the retina of mice diabetic or galactose-fed for 2 months, and are compared to those obtained from hyperglycemic rats. Methods. Diabetes was induced in mice (C57BL/6) and rats (Sprague Dawley) by alloxan injection, and experimental galactosemia by feeding normal animals diets supplemented with 30% galactose. After 2 months of hyperglycemia, levels of lipid peroxides, glutathione, nitric oxides and sorbitol, and activities of protein kinase C and (Na-K)-ATPase were measured in the retina. Results. Two months of diabetes or experimental galactosemia in mice increased retinal oxidative stress, PKC activity and nitric oxides by 40-50% and sorbitol levels by 3 folds, and these abnormalities were similar to those observed in the retina of rats hyperglycemic for 2 months. Conclusions. Metabolic abnormalities, which are postulated to play important role in the development of diabetic retinopathy in other animal models, are present in the retina of diabetic mice, and the level of metabolic abnormalities is very comparable between mice and rats. Thus, mouse seems to be a promising animal model to study the pathogenesis of diabetic retinopathy.