ArticleNeurochemical research2016
The Ketone Body, β-Hydroxybutyrate Stimulates the Autophagic Flux and Prevents Neuronal Death Induced by Glucose Deprivation in Cortical Cultured Neurons.
Article in Neurochemical research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
56 citing papers in PubMed, 1 synthesis or guideline pooled it, 108 citations in OpenAlex.
- Pooled it
- Effect of withholding early parenteral nutrition in PICU on ketogenesis as potential mediator of its outcome benefit.Critical care (London, England) · 2020Trial
- A Dose-Response Study on Human FGF21 to Inhibit Necrosis, Spectrin Breakdown, and to Increase Intracellular Cold Shock Proteins in Cultured Cortical Neurons Subjected to Oxygen-Glucose Deprivation Injury.Molecular neurobiology · 2026Article
- Autophagy-Lysosomal Axis Stimulation by Beta-Hydroxybutyrate in Astrocytes.Molecular neurobiology · 2026Article
- β-hydroxybutyrate Modulates Neuroinflammatory Responses and Astrocyte Reactivity in an In Vitro Model of Traumatic Brain Injury.Molecular neurobiology · 2026Article
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- Chronic Ketosis Provides Neuroprotection Through HIF- 1α-Mediated Control of the TXNIP/NLRP3 Axis by Regulating the Inflammatory and Apoptotic Response.Molecular neurobiology · 2025Article
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- Intermittent fasting reduces alpha-synuclein pathology and functional decline in a mouse model of Parkinson's disease.Nature communications · 2025Article
- Ketogenic diet induces an inflammatory reactive astrocytes phenotype reducing glioma growth.Cellular and molecular life sciences : CMLS · 2025Article
- β-hydroxybutyrate is a metabolic regulator of proteostasis in the aged and Alzheimer disease brain.Cell chemical biology · 2025Article
- Ketogenic Diet and Progression of Kidney Disease in Animal Models of Nephropathic Cystinosis.Journal of the American Society of Nephrology : JASN · 2024Article
- β-hydroxybutyrate and ischemic stroke: roles and mechanisms.Molecular brain · 2024Review
- Neuroprotective effects of lactate and ketone bodies in acute brain injury.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024Review
- Dietary restriction in senolysis and prevention and treatment of disease.Critical reviews in food science and nutrition · 2024Review
- Molecular Mechanisms of Neuroprotection by Ketone Bodies and Ketogenic Diet in Cerebral Ischemia and Neurodegenerative Diseases.International journal of molecular sciences · 2023Review
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Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glucose is the major energy substrate in brain, however, during ketogenesis induced by starvation or prolonged hypoglycemia, the ketone bodies (KB), acetoacetate and β-hydroxybutyrate (BHB) can substitute for glucose. KB improve neuronal survival in diverse injury models, but the mechanisms by which KB prevent neuronal damage are still not well understood. In the present study we have investigated whether protection by the D isomer of BHB (D-BHB) against neuronal death induced by glucose deprivation (GD), is related to autophagy. Autophagy is a lysosomal-dependent degradation process activated during nutritional stress, which leads to the digestion of damaged proteins and organelles providing energy for cell survival. Results show that autophagy is activated in cortical cultured neurons during GD, as indicated by the increase in the levels of the lipidated form of the microtubule associated protein light chain 3 (LC3-II), and the number of autophagic vesicles. At early phases of glucose reintroduction (GR), the levels of p62 declined suggesting that the degradation of the autophagolysosomal content takes place at this time. In cultures exposed to GD and GR in the presence of D-BHB, the levels of LC3-II and p62 rapidly declined and remained low during GR, suggesting that the KB stimulates the autophagic flux preventing autophagosome accumulation and improving neuronal survival.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.