The effects of genistein supplementation on fructose induced insulin resistance, oxidative stress and inflammation.

AIMS: This experimental study was designed to investigate the effects of 10weeks genistein administration on oxidative stress and inflammation in serum and liver of rats fed with fructose.

MAIN METHODS: 6-8weeks old, 40 male Sprague-Dawley rats were included. Group 1 (control) was fed with standard chow food and 100μl/kg/day/rat dimethyl sulfoxide (DMSO) administered subcutaneously; group 2 (genistein) with standard chow food and 0.25mg/kg/day/rat genistein; group 3 (fructose) with standard chow food and drinking water 20% fructose, group 4 (fructose+genistein) with standard chow food, drinking water with 20% fructose and 0.25mg/kg/day/rat genistein. TNF-α, IL-6, visfatin as inflammatory markers and 8-isoprostane as a oxidative stress marker were measured by ELISA, glucose, triglyceride, total cholesterol, LDL-cholesterol and HDL-cholesterol by enzymatic colorimetric method, AST and ALT by kinetic UV method.

KEY FINDINGS: Significantly high 8-isoprostane levels in serum (p<0.001) and liver (p<0.05) in group 3 compared to control group indicate that presence of oxidative stress. Significantly high TNF-α and IL-6 levels in serum (p<0.05) and liver (p<0.01) and visfatin levels in serum (p<0.001) of group 3 indicate inflammation accompanying insulin resistance and oxidative stress. Genistein administration to fructose group causes a significant decrease in HOMA-IR (p<0.001) and LDLC (p<0.05) level. Significantly lower serum 8-isoprostane (p<0.01) level indicates the antioxidant effect of genistein and significantly lower liver TNF-α (p<0.01), serum, liver IL-6(p<0.01) and serum visfatin (p<0.01) levels reflect the antiinflammatory effects of genistein.

SIGNIFICANCE: Genistein administration to rats fed with fructose causes an ameliorating effect on HOMA-IR values and lipid status markers in addition to its antioxidant and antiinflammatory effects.