Evidence map›Paper›PMID 25848768›Full record

ArticlePloS one2015

Ketones prevent oxidative impairment of hippocampal synaptic integrity through KATP channels.

Do Young Kim, Mohammed G Abdelwahab, Soo Han Lee, Derek O'Neill, Roger J Thompson, Henry J Duff, Patrick G Sullivan, Jong M Rho

Abstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

42 citing papers in PubMed.

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  18. Ketogenic diet experience at Ondokuz Mayıs University.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2021
    Article
  19. Analysis of KThe Malaysian journal of medical sciences : MJMS · 2021
    Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Do Young KimDepartments of Neurology and Neurobiology, Barrow Neurological Institute, St. Joseph's Hospital & Medical Center, Phoenix, Arizona, United States of America.
Mohammed G AbdelwahabDepartments of Neurology and Neurobiology, Barrow Neurological Institute, St. Joseph's Hospital & Medical Center, Phoenix, Arizona, United States of America.
Soo Han LeeDepartments of Neurology and Neurobiology, Barrow Neurological Institute, St. Joseph's Hospital & Medical Center, Phoenix, Arizona, United States of America.
Derek O'NeillDepartments of Neurology and Neurobiology, Barrow Neurological Institute, St. Joseph's Hospital & Medical Center, Phoenix, Arizona, United States of America.
Roger J ThompsonDepartments of Cell Biology and Anatomy, Hotchkiss Brain Institute, University of Calgary, Calgary, Alberta, Canada.
Henry J DuffLibin Cardiovascular Institute of Alberta, University of Calgary, Calgary, Alberta, Canada.
Patrick G SullivanSpinal Cord and Brain Injury Research Center, University of Kentucky, Lexington, Kentucky, United States of America.
Jong M RhoDepartments of Pediatrics and Clinical Neurosciences, Alberta Children's Hospital, Calgary, Alberta, Canada.

Funding

Metabolic Mechanisms of Functional Neuroprotection in Epileptic BrainR01NS070261 · NINDS · ST. JOSEPH'S HOSPITAL AND MEDICAL CENTER · PI KIM, DO YOUNG · 2010 to 2014
$1.6M
Canadian Institutes of Health ResearchNINDS NIH HHS NS 070261NINDS NIH HHS R01 NS070261
6 · The paper itself

Abstract

Dietary and metabolic therapies are increasingly being considered for a variety of neurological disorders, based in part on growing evidence for the neuroprotective properties of the ketogenic diet (KD) and ketones. Earlier, we demonstrated that ketones afford hippocampal synaptic protection against exogenous oxidative stress, but the mechanisms underlying these actions remain unclear. Recent studies have shown that ketones may modulate neuronal firing through interactions with ATP-sensitive potassium (KATP) channels. Here, we used a combination of electrophysiological, pharmacological, and biochemical assays to determine whether hippocampal synaptic protection by ketones is a consequence of KATP channel activation. Ketones dose-dependently reversed oxidative impairment of hippocampal synaptic integrity, neuronal viability, and bioenergetic capacity, and this action was mirrored by the KATP channel activator diazoxide. Inhibition of KATP channels reversed ketone-evoked hippocampal protection, and genetic ablation of the inwardly rectifying K+ channel subunit Kir6.2, a critical component of KATP channels, partially negated the synaptic protection afforded by ketones. This partial protection was completely reversed by co-application of the KATP blocker, 5-hydoxydecanoate (5HD). We conclude that, under conditions of oxidative injury, ketones induce synaptic protection in part through activation of KATP channels.

Indexed as

Adenosine TriphosphateAnimalsHippocampusHydrogen PeroxideIon Channel GatingKATP ChannelsKcnj11 ChannelKetonesLong-Term PotentiationMiceMice, KnockoutMitochondriaNeuronal PlasticityNeuroprotective AgentsOxidantsPatch-Clamp TechniquesAdenosine TriphosphateHydrogen PeroxideKATP ChannelsKcnj11 ChannelKetonesNeuroprotective AgentsOxidantsPotassium Channels, Inwardly RectifyingSulfonylurea Receptors

Identifiers

PMID25848768
PMCPMC4388385

What OpenQuestion holds

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LicenceCC BY
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Registered trials

None linked

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.