İskender, HaticeYenice, GülerTerim Kapakın, Kübra AsenaDokumacıoğlu, EdaÇiğdem, SevimHayırlı, Armağan2021-03-122021-03-122021İskender, H., Yenice, G., Terim Kapakın, K. A., Dokumacıoğlu, E., Sevim, C., Hayırlı, A., & Altun, S. (2021). Effects of high fructose diet on lipid metabolism and the hepatic NF-κB/SIRT-1 pathway. Biotechnic & Histochemistry,https://doi.org/10.1080/10520295.2021.1890214https://hdl.handle.net/11494/2722The liver is the primary site for fructose metabolism; therefore, the liver is susceptible to fructose related metabolic disturbances including metabolic insulin dysfunction, dyslipidemia and inflammation. We investigated whether astaxanthin (ASX) can modify hepatic nuclear factorkappa B (NF-?B)/sirtuin-1 (SIRT-1) expression to alter oxidative stress caused by ingestion of excess fructose in rats. The animals were divided randomly into two x two factorially arranged groups: two regimens were given either water (W) or 30% fructose in drinking water (F). These two groups were divided further into two subgroups each: two treatments, either orally with 0.2 ml olive oil (OO) or 1 mg ASX/kg/day in 0.2 ml olive oil (ASX). Fructose administration increased serum glucose, triglycerides and very low density lipoproteins, and decreased serum concentration of high density lipoproteins; fructose did not alter serum total cholesterol. Excess fructose decreased hepatic superoxide dismutase (SOD) and increased hepatic NF-?B and MDA levels. ASX treatment increased hepatic SIRT-1 and decreased hepatic NF-?B and malondialdehyde (MDA) levels. ASX treatment decreased hepatic NF-?B and increased SOD levels, but did not alter MDA level in rats fed high fructose. ASX administration ameliorated oxidative stress caused by excess fructose by increasing hepatic NF-?B and SIRT-1 expression.eninfo:eu-repo/semantics/closedAccessAstaxanthinFructoseLipidLiverMetabolismNF–κBOxidative stressRatsSIRT–1ArticleArticle in pres10.1080/10520295.2021.1890214Q2Q4