Impact of obesity on the brain and dietary intervention with bamboo extract

Abstract

Obesity is a worldwide public health challenge. It is associated with an array of diseases such as type 2 diabetes, cardiovascular diseases, and certain types of cancer. However, the impacts of obesity on the brain have not been sufficiently investigated. This project aimed to characterize the influences of obesity on the redox status and the function of the brain, as well as the interventional effects of dietary supplement of bamboo extract (BEX). High fat diet is a major causative factor of obesity in human, and therefore in this study we treated C57BL/6J and CD-1 mice with a high fat diet (45% calories from fat) to increase bodyweight gain. A standard diet (10% calories from fat) was used as a control. In order to study the interventional effects of BEX, this natural product was supplemented to both high fat and standard diets at a dosage of 11 g dry mass per 4057 Kcal. Lipid peroxidation and glutathione (GSH)-centered antioxidant systems were studied in the brain of the C57BL/6J mice after 6 months of dietary treatment. Anxiety-and depression-like neurobehaviors were evaluated in the CD-1 mice after 2 months of dietary treatment. The major findings of this study include: (1) When treated with the standard diet, cortex showed higher activities of glutathione-s-transferase (GST) and glutathione peroxidase (GPx), and lower level of hydroxynonenal-histidine (HNE-His, lipid peroxidation marker) in comparison to thalamus and midbrain, implicating a lower baseline of oxidative stress and higher baseline antioxidant defense ability in this brain region. (2) High fat diet-induced redox changes in the brain are region-dependent. In comparison to thalamus and midbrain, cortex is more susceptible to high fat diet-induced lipid peroxidation as indicated by the increase of HNE-His. This oxidative stress co-occurred with upregulations of GSH concentration and GST activity, signifying important antioxidant defense function of GSH and GST in cortex under obese condition. (3) When forebrain and hindbrain were concerned, the mice treated with high fat diet showed the highest GSH level and the lowest HNE-His content, implicating a potential over-compensatory mechanism to the initial insults from the high fat treatment. BEX supplement in the high fat diet abolished these changes. (4) High fat diet treatment resulted in elevated anxiety but reduced depression in the mice. BEX supplement effectively ameliorated the increases of anxiety, but showed no conclusive effects on depression. In summary, this project demonstrated that high fat diet has significant impacts on the redox status and the function of the brain. GSH and GSH-related enzymes have significant roles in antioxidant defense in the brain under both normal and obese conditions. BEX supplement effectively ameliorates high fat diet-induced redox shifting and anxiety, suggesting this cost-effective natural product has the potential to regulate the link between obesity and the brain.