Effects of high fructose diet on lipid metabolism and the hepatic NF-κB/ SIRT-1 pathway

The 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 factor-kappa B (NF-kappa 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-kappa B and MDA levels. ASX treatment increased hepatic SIRT-1 and decreased hepatic NF-kappa B and malondialdehyde (MDA) levels. ASX treatment decreased hepatic NF-kappa 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-kappa B and SIRT-1 expression.

Automated summary

The study showed that astaxanthin can alleviate oxidative stress caused by excess fructose by regulating NF-kappa B/SIRT-1 expression. Excess fructose intake resulted in elevated levels of blood glucose, triglycerides, and very low density lipoproteins, while decreasing high density lipoproteins.