Abstract
Rats fed a galactose-rich diet have been used for several years as a model for diabetes to study, particularly in the eye, the effects of excess blood hexoses. This study sought to determine the utility of galactosemia as a model for oxidative stress in extraocular tissues by examining biomarkers of oxidative stress in galactose-fed rats and experimentally-induced diabetic rats. Sprague-Dawley rats were divided into four groups: experimental control; streptozotocin-induced diabetic; insulin-treated diabetic; and galactose-fed. The rats were maintained on these regimens for 30 days, at which point the activities of catalase, glutathione peroxidase, glutathione reductase, and superoxide dismutase, as well as levels of lipid peroxidation and reduced and oxidized glutathione were determined in heart, liver, and kidney. This study indicates that while there are some similarities between galactosemic and diabetic rats in these measured indices of oxidative stress (hepatic catalase activity levels and hepatic and renal levels of oxidized glutathione in both diabetic and galactosemic rats were significantly decreased when compared to normal), overall the galactosemic rat model is not closely parallel to the diabetic rat model in extra-ocular tissues. In addition, several effects of diabetes (increased hepatic glutathione peroxidase activity, increased superoxide dismutase activity in kidney and heart, decreased renal and increased cardiac catalase activity) were not mimicked in galactosemic rats, and glutathione concentration in both liver and heart was affected in opposite ways in diabetic rats and galactose- fed rats. Insulin treatment reversed/prevented the activity changes in renal and cardiac superoxide dismutase, renal and cardiac catalase, and hepatic glutathione peroxidase as well as the hepatic changes in lipid peroxidation and reduced and oxidized glutathione, and the increase in cardiac glutathione. Thus, prudence should be exercised in the use of experimentally galactosemic rats as a model for diabetes until the correspondence of the models has been more fully characterized.
Highlights
The defining property of diabetes mellitus (DM) is the inability of the body to regulate glucose metabolism
I71 For nearly two decades, experimentally induced hypergalactosemia has been used as a model to study the morphological and biochemical changes that retinal tissue undergoes as a result of high.blood sugars.I8,91 The retinopathy that develops under these conditions is morphologically similar to that which occurs in diabetes,I1,11 and the stability of the hypergalactosemic state facilitates long-term studies, which are difficult in experimentally diabetic animals
The galactosemic rats showed no significant increase or decrease in blood glucose, but the apparent increase in HbAlc was not significant at p < 0.05. In retrospect this is plausible because, while glycosylation secondary to excess glucose is best measured with HbAlc, the glycosylation secondary to galactosemia is more detectable on the HbAla and HbAlb fractions.[21 Insulin treatment reversed/prevented the diabetes-induced changes in body weight, liver/body weight ratio, serum glucose concentrations and HbAlc levels
Summary
The defining property of diabetes mellitus (DM) is the inability of the body to regulate glucose metabolism This inability arises as a result of either insufficient or nonexistent insulin production, as in Type I DM, or tissue insensitivity to insulin, as in Type II DM. I71 For nearly two decades, experimentally induced hypergalactosemia has been used as a model to study the morphological and biochemical changes that retinal tissue undergoes as a result of high.blood sugars.I8,91 The retinopathy that develops under these conditions is morphologically similar to that which occurs in diabetes,I1,11 and the stability of the hypergalactosemic state facilitates long-term studies, which are difficult in experimentally diabetic animals. This study hypothesizes that focusing solely on excess hexose, as in experimental galactosemia, does not provide a reasonable model of the oxidative stresses experienced in various tissues by diabetic rats
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