Abstract
Obesity induces serious diseases such as diabetes and cardiovascular disease. It has been reported that obesity increases the risk of cognitive dysfunction. Cognitive dysfunction is a characteristic symptom of Alzheimer’s and Parkinson’s diseases. However, the detailed mechanisms of obesity-induced cognitive dysfunction have not yet been elucidated. The onset and progression of obesity-induced severe secondary diseases such as diabetes, cardiovascular events, and hypertension are deeply connected to oxidative stress. We hypothesized that obesity induces cognitive dysfunction via acceleration of reactive oxygen species (ROS) production. Vitamin E, which is a lipophilic vitamin, has strong antioxidative effects and consists of two groups: tocopherols and tocotrienols. Recently, it has been demonstrated that tocotrienols have strong neuroprotective and anti-obesity effects. In this study, we fed mice a high-fat diet (HFD) from 9 to 14 months of age and assessed the effect of tocotrienols treatment on body weight, brain oxidation levels, and cognitive function. The results revealed that treatment with tocotrienols inhibited body weight gain; further, tocotrienols reached the brain and attenuated oxidation in HFD-treated mice. These results indicate that tocotrienols have anti-obesity effects and inhibit obesity-induced brain oxidation.
Highlights
The number of people with obesity continues to increase throughout the world [1]
The results indicated that sufficient levels of TOCs and T3s were included in each diet, with the exception of β-TOC (Figure 1)
Co-treatment with high-fat diet (HFD) and T3s tended to inhibit the body weight gain compared to the HFD group until 10 weeks, and the ratio of body weight gain of both control diet (CD) groups were similar until 14
Summary
The number of people with obesity continues to increase throughout the world [1]. It is well known that the body mass index (BMI, body weight (kg)/square of body height (m)) score is used as the primary index of obesity. Several lines of evidence have identified the relationship between obesity and the onset and progression of cognitive dysfunction. It has been reported that the onset and progression of these neurodegenerative disorders are related to oxidative damage regardless of obesity [6], the detailed mechanisms of obesity-related cognitive dysfunction have not yet been elucidated. Calorie restriction (CR) in mice and rhesus monkeys has shown life span extension via autophagy activation and attenuation of oxidative stress [8,9]. Based on this background information, we propose hypotheses regarding obesity-derived cognitive dysfunction. Obesity may induce cognitive dysfunction via accumulation of brain oxidation. Treatment with antioxidant substances, such as vitamin E (VE), may play a beneficial role in obesity-related oxidative damage
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