Abstract
Excess fructose consumption can lead to metabolic syndrome, including insulin resistance, dyslipidemia, and hepatic injury, which are associated with oxidative stress and inflammation. The present study was to investigate whether fisetin improved multiple disturbances induced by fructose consumption. First, fisetin was found to be nontoxic to mice after an 8 week treatment. Second, the mice fed with a high-fructose (HFru)-diet for 8 weeks exhibited insulin resistance, dyslipidemia, hepatic injury, oxidative stress, and inflammation. Fisetin supplementation effectively improved the undesirable results mentioned above when compared to the HFru group. Meanwhile, fisetin significantly suppressed the nuclear factor κ-light-chain-enhancer of activated B cells (NF-κB) pathway and activated the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway in mice fed with HFru. Our findings demonstrated that fisetin exerted the beneficial effects in HFru-feeding mice, which might be associated with suppression of NF-κB and activation of the Nrf2 pathway.
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