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

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dc.contributor.authorArmucu, Ferah
dc.contributor.authorKanter, Mehmet
dc.contributor.authorGuerel, Ahmet
dc.contributor.authorUnalacak, Murat
dc.date.accessioned2024-06-12T11:02:19Z
dc.date.available2024-06-12T11:02:19Z
dc.date.issued2007
dc.departmentTrakya Üniversitesien_US
dc.description.abstractObjective: Drinking large amounts of carbonated beverage is associated with increased risk for obesity and nonalcoholic steato-hepatitis. 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.en_US
dc.identifier.endpage169en_US
dc.identifier.issn1300-0292
dc.identifier.issn2146-9040
dc.identifier.issue2en_US
dc.identifier.scopus2-s2.0-34547485398en_US
dc.identifier.scopusqualityQ4en_US
dc.identifier.startpage164en_US
dc.identifier.urihttps://hdl.handle.net/20.500.14551/21232
dc.identifier.volume27en_US
dc.identifier.wosWOS:000254582300002en_US
dc.identifier.wosqualityN/Aen_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.language.isoenen_US
dc.publisherOrtadogu Ad Pres & Publ Coen_US
dc.relation.ispartofTurkiye Klinikleri Tip Bilimleri Dergisien_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectFructoseen_US
dc.subjectFatty Liveren_US
dc.subjectLipid Peroxidationen_US
dc.subjectRatsen_US
dc.subjectOxidative Stressen_US
dc.subjectCopper Deficiencyen_US
dc.subjectImprovesen_US
dc.subjectConsumptionen_US
dc.subjectMetabolismen_US
dc.subjectDefenseen_US
dc.subjectOxidaseen_US
dc.titleExcessive dietary fructose is responsible for lipid peroxidation and steatosis in the rat liver tissuesen_US
dc.typeArticleen_US

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