Long-term fructose-enriched diet introduced immediately after weaning does not induce oxidative stress in the rat liver

Increased fructose consumption is correlated with the rising prevalence of obesity, metabolic syndrome, and type 2 diabetes. It is believed that reactive oxygen species contribute to the development and progression of metabolic disturbances, especially those associated with insulin resistance. Dietary fructose produces both pro-oxidative and antioxidative effects, depending upon the experimental conditions, dosage, duration of treatment, and pathophysiological milieu. The effects of fructose overconsumption on young populations, which have an increased risk of developing metabolic disorders in adulthood, have not been fully elucidated. We have previously shown that rats subjected to a long-term fructose-enriched diet immediately after weaning display impaired hepatic insulin sensitivity. In this study, we tested the hypothesis that long-term fructose consumption induces alterations in the redox setting of the liver. Starting from the 21st day after birth, male Wistar rats were maintained for 9 weeks on a standard diet (control) or a fructose-enriched diet that consisted of standard food and 10% fructose solution instead of drinking water. The expression and activity of antioxidant enzymes as well as lipid peroxidation and protein damage markers were measured. The results showed that a fructose-enriched diet led to an increased expression of mitochondrial manganese superoxide dismutase but did not affect antioxidant enzymes activity, lipid peroxidation, thiol content, and the level of protein oxidation. Therefore, our results suggest that the decrease in hepatic insulin sensitivity that was previously observed in rats that were kept on the same diet regime might be attributed to molecular mechanisms other than redox disbalance. A possible fructose-related micronutrient deficiency should be examined.