ArticleMolecular neurobiology2018
High-Fructose Consumption Impairs the Redox System and Protein Quality Control in the Brain of Syrian Hamsters: Therapeutic Effects of Melatonin.
Article in Molecular neurobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 28 citations in OpenAlex.
- Loss of melatonin signaling increases the risk of T2DM caused by metabolic disorders.Cell communication and signaling : CCS · 2025Article
- High-fructose diet induces depressive-like behaviors and short-term memory deficits through hippocampal neurogenesis impairment via neural stem cell dysfunction.Nutrition & metabolism · 2025Article
- Differential Cellular Interactome in Schizophrenia and Bipolar Disorder-Discriminatory Biomarker Role.Antioxidants (Basel, Switzerland) · 2023Article
- Fructose Diet-Associated Molecular Alterations in Hypothalamus of Adolescent Rats: A Proteomic Approach.Nutrients · 2023Article
- Removal of Environmental Nanoparticles Increases Protein Synthesis and Energy Production in Healthy Humans.Frontiers in bioengineering and biotechnology · 2022Article
- Melatonin induces the rejuvenation of long-term ex vivo expanded periodontal ligament stem cells by modulating the autophagic process.Stem cell research & therapy · 2021Article
- Review
- Rheostatic Balance of Circadian Rhythm and Autophagy in Metabolism and Disease.Frontiers in cell and developmental biology · 2020Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Although numerous studies have demonstrated the harmful effect of excessive fructose consumption at the systemic level, there is little information on its effects in the central nervous system. The purpose of the present work was to study the cellular alterations related to oxidative stress and protein quality control systems induced by a high-fructose diet in the brain of Syrian hamsters and their possible attenuation by exogenous melatonin. High-fructose intake induced type II diabetes together with oxidative damage, led to alterations of the unfolded protein response by activating the eIF2α branch, and impaired the macroautophagic machinery in the brain, favoring the accumulation of aggregates labeled for selective degradation and neurodegeneration markers such as β-amyloid (1-42), tau-p-S199, and tau-p-S404. Melatonin attenuated the manifestation of type II diabetes and reduced oxidative stress, deactivated eIF2α, and decreased tau-p-S404 levels in the brain of animals fed a high-fructose diet.
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Registered trials
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