Evidence map›Paper›PMID 31993694›Full record

ArticlePsychopharmacology2020

Effects of beta-hydroxybutyrate administration on MK-801-induced schizophrenia-like behaviour in mice.

Ann-Katrin Kraeuter, Tadiwa Mashavave, Aditya Suvarna, Maarten van den Buuse, Zoltán Sarnyai

Abstract read
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Article in Psychopharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.5field-weighted citation impact, top 7% of its field
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

36 citing papers in PubMed, 55 citations in OpenAlex.

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  19. [Ursolic acid improved demyelination and interstitial fluid drainage disorders in schizophrenia mice].Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2024
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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

5 authors at 2 institutions in 1 country.

Ann-Katrin KraeuterLaboratory of Psychiatric Neuroscience, Australian Institute of Tropical Health and Medicine, Douglas, Australia.
Tadiwa MashavaveLaboratory of Psychiatric Neuroscience, Australian Institute of Tropical Health and Medicine, Douglas, Australia.
Aditya SuvarnaLaboratory of Psychiatric Neuroscience, Australian Institute of Tropical Health and Medicine, Douglas, Australia.
Maarten van den BuuseCollege of Public Health, Medical and Veterinary Sciences, James Cook University, Townsville, Queensland, Australia.
Zoltán SarnyaiLaboratory of Psychiatric Neuroscience, Australian Institute of Tropical Health and Medicine, Douglas, Australia. zoltan.sarnyai@jcu.edu.au.ORCID http://orcid.org/0000-0002-2380-7902
Australian Institute of Tropical Health and Medicine · AULa Trobe University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

rationaleImpaired cerebral glucose metabolism is a core pathological feature of schizophrenia. We recently demonstrated that a ketogenic diet, causing a shift from glycolysis to ketosis, normalized schizophrenia-like behaviours in an acute N-methyl-D-aspartate (NMDA) receptor antagonist model of the illness. Ketogenic diet produces the ketone body, β-hydroxybutyrate (BHB), which may serve as an alternative fuel source in its own right without a strict dietary regime.

objectiveWe hypothesized that chronic administration of BHB replicates the therapeutic effects of ketogenic diet in an acute NMDA receptor hypofunction model of schizophrenia in mice.

methodsC57Bl/6 mice were either treated with acute doses of 2 mmol/kg, 10 mmol/kg, or 20 mmol/kg BHB or received daily intraperitoneal injections of 2 mmol/kg BHB or saline for 3 weeks. Behavioural testing assessed the effect of acute challenge with 0.2 mg/kg MK-801 or saline on open field behaviour, social interaction, and prepulse inhibition of startle (PPI).

resultsAcute BHB administration dose-dependently increased BHB plasma levels, whereas the 2 mmol/kg dose increased plasma glucose levels. The highest acute dose of BHB supressed spontaneous locomotor activity, MK-801-induced locomotor hyperactivity and MK-801-induced disruption of PPI. Chronic BHB treatment normalized MK-801-induced hyperlocomotion, reduction of sociability, and disruption of PPI.

conclusionIn conclusion, BHB may present a novel treatment option for patients with schizophrenia by providing an alternative fuel source to normalize impaired glucose metabolism in the brain.

Indexed as

3-Hydroxybutyric AcidAnimalsDizocilpine MaleateDose-Response Relationship, DrugExcitatory Amino Acid AntagonistsInjections, IntraperitonealLocomotionMaleMiceMice, Inbred C57BLMotor ActivityPrepulse InhibitionReceptors, N-Methyl-D-AspartateReflex, StartleSchizophreniaTreatment Outcome3-Hydroxybutyric AcidDizocilpine MaleateExcitatory Amino Acid AntagonistsReceptors, N-Methyl-D-AspartateBeta-hydroxybutyrate (BHB)Ketogenic dietMK-801N-Methyl-D-aspartate (NMDA) receptor hypofunctionSchizophreniaSensorimotor gatingSociability

Identifiers

PMID31993694
OpenAlexW3003218876

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.