Abstract
Obesity is a serious public health issue in developed countries, and is known to increase the risk of several diseases such as diabetes, cardiovascular events and arteriosclerosis. These phenomena are closely correlated with oxidative damage. Recently, several lines of evidence have demonstrated that neurodegenerative diseases such as Alzheimer’s and Parkinson’s are also related to oxidative damage. To clarify the relationship between obesity and oxidative brain injury, we investigated brain antioxidant networks in high-fat (HF) diet-treated mice in the presence or absence of tocotrienols (T3s) and bran. Co-treatment with T3s and bran significantly inhibited bodyweight gain in HF diet-treated mice. Serum and cortex T3 levels, and brain antioxidant enzyme activities and protein expressions did not differ among the groups except for SOD protein expression in the cerebellum. Brain p-mTOR and p-Akt protein expressions, which are related to autophagy, did not differ among the groups. These results indicate that treatment with T3s for eight weeks had showed an anti-obesity effect in HF diet-treated mice. However, significant alterations in T3 levels were not observed in the serum and brain of mice.
Highlights
Obesity is a serious global issue [1,2] that is characterized by a high body-mass index (BMI, weight in kilograms divided by the square of the height in meters), and its incidence is gradually increasing in Japan
The majority of current studies on calorie restriction and lifespan extension employ rodents [6] and non-human primates [9], and the results indicated that sirtuin 1 expression [10], known as the “longevity gene”, and down-regulation of metabolic rate [11] play a role
superoxide dismutase (SOD) protein expression in the hippocampus tended to increase in the HF-treated group compared to the control. These results indicated that the production of oxidative stress was slightly increased in the brain by HF
Summary
Obesity is a serious global issue [1,2] that is characterized by a high body-mass index (BMI, weight in kilograms divided by the square of the height in meters), and its incidence is gradually increasing in Japan. The majority of current studies on calorie restriction and lifespan extension employ rodents [6] and non-human primates [9], and the results indicated that sirtuin 1 expression [10], known as the “longevity gene”, and down-regulation of metabolic rate [11] play a role. Reduced oxygen consumption is a key factor in calorie restriction-related lifespan extension [12]; in other words, obesity patients may exhibit high oxygen consumption, possibly shortening their lifespan. Reactive oxygen species (ROS)-derived oxidative damage accelerates pathological aging, known as “the free radical theory of aging” [13], and increases the risk of the development and progression of severe diseases, such as neurodegenerative disorders [14,15]. The detailed relationship between ROS-derived oxidative damage in the brain and obesity has not been elucidated
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