LAUSR

Obesity is increasing in developed countries and is well known to a risk factor of severe diseases such as diabetes and Alzheimer's disease. Several kinds of evidence have been demonstrated that these diseases relate to oxidative damage. However, the detailed mechanisms of it relation have not yet elucidated. Previously, we reported that cognitive dysfunction is induced in normal aged- and vitamin E (V.E)-deficient mice models via accumulation of brain oxidation. On the basis of these data, we hypothesized that obesity increased the risk of cognitive dysfunction via brain oxidation. Tocotrienols (T3s) which are one kind of vitamin E have many biological functions. The most famous function of T3s is antioxidant, and the function is stronger than that of tocopherols. Other beneficial function of T3s is neuroprotection and inhibitory effect of HMG-CoA reductase. In this study, we assessed motor and cognitive function of long- and short-term high-fat diet-treated mice in the presence or absence of T3s. Furthermore, we measured V.E, TBARS and antioxidant enzyme activity in these mice liver, serum and brain. These results indicate that obesity induce cognitive dysfunction via brain oxidation and treatment with T3s may show anti-obesity and neuroprotective effect in our model.