Difference between revisions of "Mazzoli 2021 Antioxidants (Basel)"
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{{Publication | {{Publication | ||
|title=Mazzoli A, Spagnuolo MS, Nazzaro M, Gatto C, Iossa S, Cigliano L (2021) Fructose removal from the diet reverses inflammation, mitochondrial dysfunction, and oxidative stress in hippocampus . Antioxidants (Basel) 10:487. | |title=Mazzoli A, Spagnuolo MS, Nazzaro M, Gatto C, Iossa S, Cigliano L (2021) Fructose removal from the diet reverses inflammation, mitochondrial dysfunction, and oxidative stress in hippocampus. Antioxidants (Basel) 10:487. | ||
|info=[https://pubmed.ncbi.nlm.nih.gov/33804637 PMID: 33804637 Open Access] | |info=[https://pubmed.ncbi.nlm.nih.gov/33804637 PMID: 33804637 Open Access] | ||
|authors=Mazzoli Arianna, Spagnuolo Maria Stefania, Nazzaro Martina, Gatto Cristina, Iossa Susanna, Cigliano Luisa | |authors=Mazzoli Arianna, Spagnuolo Maria Stefania, Nazzaro Martina, Gatto Cristina, Iossa Susanna, Cigliano Luisa | ||
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|keywords=PSD-95, Fructose diet, Haptoglobin, Hippocampus, Inflammation, Mitochondria, Neurofilament-M, Oxidative stress, Young rat | |keywords=PSD-95, Fructose diet, Haptoglobin, Hippocampus, Inflammation, Mitochondria, Neurofilament-M, Oxidative stress, Young rat | ||
|editor=[[Plangger M]] | |editor=[[Plangger M]] | ||
|mipnetlab=IT Naples Iossa S | |||
}} | }} | ||
{{Labeling | {{Labeling | ||
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|organism=Rat | |organism=Rat | ||
|tissues=Nervous system | |tissues=Nervous system | ||
|preparations=Homogenate | |||
|couplingstates=LEAK, OXPHOS, ET | |||
|pathways=N, S, NS, ROX | |||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
|additional=2021-07 | |additional=2021-07 | ||
}} | }} |
Latest revision as of 13:29, 12 July 2021
Mazzoli A, Spagnuolo MS, Nazzaro M, Gatto C, Iossa S, Cigliano L (2021) Fructose removal from the diet reverses inflammation, mitochondrial dysfunction, and oxidative stress in hippocampus. Antioxidants (Basel) 10:487. |
Mazzoli Arianna, Spagnuolo Maria Stefania, Nazzaro Martina, Gatto Cristina, Iossa Susanna, Cigliano Luisa (2021) Antioxidants (Basel)
Abstract: Young age is often characterized by high consumption of processed foods and fruit juices rich in fructose, which, besides inducing a tendency to become overweight, can promote alterations in brain function. The aim of this study was therefore to (a) clarify brain effects resulting from fructose consumption in juvenile age, a critical phase for brain development, and (b) verify whether these alterations can be rescued after removing fructose from the diet. Young rats were fed a fructose-rich or control diet for 3 weeks. Fructose-fed rats were then fed a control diet for a further 3 weeks. We evaluated mitochondrial bioenergetics by high-resolution respirometry in the hippocampus, a brain area that is critically involved in learning and memory. Glucose transporter-5, fructose and uric acid levels, oxidative status, and inflammatory and synaptic markers were investigated by Western blotting and spectrophotometric or enzyme-linked immunosorbent assays. A short-term fructose-rich diet induced mitochondrial dysfunction and oxidative stress, associated with an increased concentration of inflammatory markers and decreased Neurofilament-M and post-synaptic density protein 95. These alterations, except for increases in haptoglobin and nitrotyrosine, were recovered by returning to a control diet. Overall, our results point to the dangerous effects of excessive consumption of fructose in young age but also highlight the effect of partial recovery by switching back to a control diet. β’ Keywords: PSD-95, Fructose diet, Haptoglobin, Hippocampus, Inflammation, Mitochondria, Neurofilament-M, Oxidative stress, Young rat β’ Bioblast editor: Plangger M β’ O2k-Network Lab: IT Naples Iossa S
Labels: MiParea: Respiration, Developmental biology, Exercise physiology;nutrition;life style
Organism: Rat
Tissue;cell: Nervous system
Preparation: Homogenate
Coupling state: LEAK, OXPHOS, ET
Pathway: N, S, NS, ROX
HRR: Oxygraph-2k
2021-07