Short-term Fructose Feeding induces Inflammation and Oxidative Stress in Hippocampus of Young and Adult Rats

The drastic increase in the consumption of fructose encouraged the research to focus on its effects on brain physio-pathology. Although young and adults differ largely by their metabolic and physiological profiles, most of the pre- vious studies investigated brain disturbances induced by long- term fructose feeding in adults. Therefore, we investigated whether a short-term consumption of fructose (2 weeks) pro- duces early increase in specific markers of inflammation and oxidative stress in the hippocampus of young and adult rats. After the high-fructose diet, plasma lipopolysaccharide and tumour necrosis factor (TNF)-alpha were found significantly increased in parallel with hippocampus inflammation, evi- denced by a significant rise in TNF-alpha and glial fibrillar acidic protein concentrations in both the young and adult groups. The fructose-induced inflammatory condition was as- sociated with brain oxidative stress, as increased levels of lipid peroxidation and nitro-tyrosine were detected in the hippo- campus. The degree of activation of the protein kinase B, extracellular signal-regulated kinase 1/2, and insulin receptor substrate 1 pathways found in the hippocampus after fructose feeding indicates that the detrimental effects of the fructose- rich diet might largely depend on age. Mitochondrial function in the hippocampus, together with peroxisome proliferator- activated receptor gamma coactivator 1-alpha content, was found significantly decreased in fructose-treated adult rats.