|Roussel, Anne - J.FOURIER U, GRENOBLE FR|
|Hininger, Isabelle - J.FOURIER U, GRENOBLE FR|
|Coves, Sara - UNILEVER, FR,F92842 RUEIL|
Submitted to: International Conference of Polyphenols
Publication Type: Proceedings
Publication Acceptance Date: October 16, 2007
Publication Date: November 25, 2007
Citation: Roussel, A., Hininger, I., Coves, S., Anderson, R.A. 2007. Tea and cinnamon polyphenols improve the metabolic syndrome. International Conference of Polyphenols. 3:506-1. Technical Abstract: Hyperglycemia and insulin resistance, key features of the metabolic syndrome, are leading causes of early brain alterations. Green tea, by a mechanism involving the improvement of insulin sensitivity and the control of oxidative stress, could be a factor of neuroprotection in insulin-resistant states like the metabolic syndrome. Our objective was to investigate the in vivo effects of green tea consumption on brain oxidative stress using an experimental rodent model of diet-induced insulin resistance, the fructose fed rat. Three groups of rats, 10 per group, were fed a semi purified Purina chow or a fructose rich diet (FD) or FD plus 1g green tea extract/kg diet for 12 weeks. Oxidative stress parameters in blood and brain were measured for lipid (TBAR’s) and protein (SH groups) oxidation, oxidized and reduced glutathione (GSH/GSSG), ferric reducing ability power (FRAP), and DNA oxidative damages (Comet assay). Behavioral activity of the animals was tested using the open-field test. FD led to increased oxidative stress compared with the control group. Addition of green tea extract to the diet resulted in significant decreases in lipid oxidation and DNA oxidative damage while plasma SH groups and GSH/GSSG remained unchanged. FRAP was enhanced. Improvements in behavioral activity, due to tea extract consumption, were not statistically significant. This study shows that green tea extract protects against brain oxidative damage and suggests possible neuroprotective effects against early brain alterations and free radical-induced neurodegenerative diseases in people with the metabolic syndrome.