Changes in cerebral cortex redox status and cognitive performance in short- and long-term high-sucrose diet fed rats

Rising evidence suggests that Metabolic Syndrome (MetS) would be correlated with the development of neurodegenerative diseases. Although this has emerged as a relevant area of research, it has not been fully explored. It is not clear if a greater impairment of the metabolic peripheral environment is accompanied by a greater impairment of the central nervous system. We have previously shown that feeding rats with a high-sucrose diet (HSD) represents an animal model that resembles the human MetS phenotype. The aim of the present work was to assess in rats fed a HSD for a short (3 weeks-wk) or a long (15 weeks-wk) term, whether the worsening of the peripheral metabolic and hormonal profile that occur as the time of HSD consumption increases, is also accompanied by a worsening of oxidative stress in the cerebral cortex and/or cognitive behavior. Male Wistar rats received a HSD or a control diet during 3 wk or 15 wk. We found an increase in reactive oxygen species (ROS), thiobarbituric acid reactive substances (TBARS), advanced glycation end products (AGEs) and glutathione peroxidase (GPx) and glutathione reductase (GR) enzyme activities in the cerebral cortex of 3 wk HSD-fed rats. All of these parameters, except for the GPx, were also increased in the 15 wk HSD-fed group and values were similar to those observed at 3 wk. Glutathione reduced form (GSH), catalase (CAT) activity and brain-to-body weight ratio were reduced in 15 wk HSD-fed animals. Glutathione S- transferase (GST) was similar in all dietary groups. A poor performance in novel object recognition test and T-maze memory tasks was observed in 3 wk and 15 wk HSD-fed rats in a similar magnitude. Our results add new evidence related to the association between an adverse peripheral metabolic environment and brain/cognitive dysfunction.