Mazzoli 2021 Antioxidants (Basel): Difference between revisions

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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

Publications in the MiPMap
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.

ยป PMID: 33804637 Open Access

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. โ€ข Keywords: PSD-95, Fructose diet, Haptoglobin, Hippocampus, Inflammation, Mitochondria, Neurofilament-M, Oxidative stress, Young rat โ€ข Bioblast editor: Plangger M โ€ข 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 

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