Excessive dietary fructose is responsible for lipid peroxidation and steatosis in the rat liver tissues

Objective: Drinking large amounts of carbonated beverage is associated with increased risk for obesity and nonalcoholic steatohepatitis. Fructose is found in many fruits, vegetables, honey and in soft drinks, such as high fructose corn syrup. Excessive fructose consumption can adversely affect liver metabolism and increase lipid peroxidation, and this plays a role in the pathology associated with fructose feeding. Material and Methods: The present study reports the effects of high-fructose diet (10% and 20% in the drinking water) on the liver lipid peroxidation of rats. At the end of the experiment, biochemical evaluation of plasma and histopathological evaluation of liver tissue were performed. Results: Enhanced thiobarbituric acid-reactant substance levels and abnormal lipid changes were observed in high-fructose-fed rats. In 10% fructose-fed group, the most consistent findings in the histologic sections of liver tissues were the hepatocellular degenerative changes, minimal macrovesicular and microvesicular steatosis in zone 1. In the 20% fructose-fed group, the trabecular liver structure was more seriously affected than the 10% fructose-fed group. High fructose-induced degenerative changes were evident in numerous hepatocytes of zone 1; the cells were enlarged and had a light and foamy cytoplasm filled with vacuoles. Conclusion: Our study suggests that fructose feeding is associated with lipid peroxidation and steatosis in liver and the dose of fructose is associated with the degree of tissue damage. Copyright © 2007 by Türkiye Klinikleri