Objective: Metabolic syndrome (MetS) can be induced by the oxidative stress conditions caused by ingestion of large amounts of fructose. We investigated the possible protective effects of melatonin administration on liver tissues in fructose-fed rats.
Materials and methods: Thirty-two rats were randomly divided into four groups; control, fructose, melatonin, and fructose plus melatonin. MetS was induced by a fructose solution (20% in tap water) and melatonin (20 mg/kg daily) was administered by oral gavage. Systolic blood pressures (SBP) were measured. After the end of the 8-week experimental period, serum lipid profile, glucose and insulin levels, tissue total oxidant status (TOS) and activities of paraoxonase (PON), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) and catalase (CAT) were measured.
Results: Fructose consumption significantly increased SBP, serum triglyceride and insulin levels and induced insulin resistance, confirming successful establishment of the MetS model. After fructose administration, the TOS levels and GSH-Px activities significantly increased in all groups compared to the control group. The PON activity in the fructose group significantly decreased compared to the control group. Melatonin supplementation, with or without fructose, increased PON activity. The SOD activity significantly increased in the fructose group compared to the control group, but significantly decreased in the melatonin group compared to the control and fructose groups. CAT activity was unchanged in all groups.
Conclusions: GSH-PX and PON are important antioxidants for reducing oxidant stress. Melatonin might act as a prooxidant at the dose given in our experimental design when administered with fructose.