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.

Short-term Fructose Feeding induces Inflammation and Oxidative Stress in Hippocampus of Young and Adult Rats / Cigliano, Luisa; Spagnuolo, MARIA STEFANIA; Crescenzo, Raffaella; Cancelliere, Rosa; Iannotta, Lucia; Mazzoli, Arianna; Liverini, Giovanna; Iossa, Susanna. - In: MOLECULAR NEUROBIOLOGY. - ISSN 0893-7648. - 55:(2018), pp. 2869-2883. [DOI: 10.1007/s12035-017-0518-2]

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

CIGLIANO, LUISA;SPAGNUOLO, MARIA STEFANIA;CRESCENZO, RAFFAELLA;CANCELLIERE, ROSA;IANNOTTA, LUCIA;MAZZOLI, ARIANNA;LIVERINI, GIOVANNA;IOSSA, SUSANNA
2018

Abstract

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.
2018
Short-term Fructose Feeding induces Inflammation and Oxidative Stress in Hippocampus of Young and Adult Rats / Cigliano, Luisa; Spagnuolo, MARIA STEFANIA; Crescenzo, Raffaella; Cancelliere, Rosa; Iannotta, Lucia; Mazzoli, Arianna; Liverini, Giovanna; Iossa, Susanna. - In: MOLECULAR NEUROBIOLOGY. - ISSN 0893-7648. - 55:(2018), pp. 2869-2883. [DOI: 10.1007/s12035-017-0518-2]
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11588/671550
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