Evidence map›Paper›PMID 28324109›Full record

ArticleEndocrinology2017

Sex-Specific Life Course Changes in the Neuro-Metabolic Phenotype of Glut3 Null Heterozygous Mice: Ketogenic Diet Ameliorates Electroencephalographic Seizures and Improves Sociability.

Yun Dai, Yuanzi Zhao, Masatoshi Tomi, Bo-Chul Shin, Shanthie Thamotharan, Andrey Mazarati, Raman Sankar, Elizabeth A Wang, Carlos Cepeda, Michael S Levine and 8 more

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

20 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Ketogenic diet for mood disorders from animal models to clinical application.Journal of neural transmission (Vienna, Austria : 1996) · 2023
    Review
  10. Review
  11. Article
  12. Diet in treatment of autism spectrum disorders.Frontiers in neuroscience · 2022
    Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Transcript Analysis of Zebrafish GLUT3 Genes,Frontiers in molecular neuroscience · 2019
    Article
  18. Neural Deletion of Glucose Transporter Isoform 3 Creates Distinct Postnatal and Adult Neurobehavioral Phenotypes.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
    Article
  19. The Antiepileptic Ketogenic Diet Alters Hippocampal Transporter Levels and Reduces Adiposity in Aged Rats.The journals of gerontology. Series A, Biological sciences and medical sciences · 2018
    Article
  20. Ketone-Based Metabolic Therapy: Is Increased NADFrontiers in molecular neuroscience · 2017
    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

18 authors at 2 institutions in 1 country.

Yun DaiDepartment of Pediatrics, Division of Neonatology & Developmental Biology, Neonatal Research Center at the UCLA Children's Discovery and Innovation Institute, Los Angeles, California, U.S.A.
Yuanzi ZhaoDepartment of Pediatrics, Division of Neonatology & Developmental Biology, Neonatal Research Center at the UCLA Children's Discovery and Innovation Institute, Los Angeles, California, U.S.A.
Masatoshi TomiDepartment of Pediatrics, Division of Neonatology & Developmental Biology, Neonatal Research Center at the UCLA Children's Discovery and Innovation Institute, Los Angeles, California, U.S.A.
Bo-Chul ShinDepartment of Pediatrics, Division of Neonatology & Developmental Biology, Neonatal Research Center at the UCLA Children's Discovery and Innovation Institute, Los Angeles, California, U.S.A.
Shanthie ThamotharanDepartment of Pediatrics, Division of Neonatology & Developmental Biology, Neonatal Research Center at the UCLA Children's Discovery and Innovation Institute, Los Angeles, California, U.S.A.
Andrey MazaratiDepartment of Pediatrics, Division of Neurology, David Geffen School of Medicine at UCLA, Los Angeles, California, U.S.A.
Raman SankarDepartment of Pediatrics, Division of Neurology, David Geffen School of Medicine at UCLA, Los Angeles, California, U.S.A.
Elizabeth A WangIntellectual and Developmental Disabilities Research Center and Brain Research Institute, David Geffen School of Medicine, Semel Institute for Neuroscience and Human Behavior, University of California Los Angeles (UCLA), Los Angeles, CA, USA.
Carlos CepedaIntellectual and Developmental Disabilities Research Center and Brain Research Institute, David Geffen School of Medicine, Semel Institute for Neuroscience and Human Behavior, University of California Los Angeles (UCLA), Los Angeles, CA, USA.
Michael S LevineIntellectual and Developmental Disabilities Research Center and Brain Research Institute, David Geffen School of Medicine, Semel Institute for Neuroscience and Human Behavior, University of California Los Angeles (UCLA), Los Angeles, CA, USA.
Jingjing ZhangDepartment of Neurology, David Geffen School of Medicine at UCLA, Los Angeles, California, U.S.A.
Andrew FrewDepartment of Neurology, David Geffen School of Medicine at UCLA, Los Angeles, California, U.S.A.
Jeffry R AlgerDepartment of Neurology, David Geffen School of Medicine at UCLA, Los Angeles, California, U.S.A.
Peter M ClarkDepartment of Molecular and Medical Pharmacology and Crump Institute for Molecular Imaging, David Geffen School of Medicine at UCLA, Los Angeles, California, USA.
Monica SondhiDepartment of Pediatrics, Division of Neonatology & Developmental Biology, Neonatal Research Center at the UCLA Children's Discovery and Innovation Institute, Los Angeles, California, U.S.A.
Sudatip KositamongkolDepartment of Pediatrics, Division of Neonatology & Developmental Biology, Neonatal Research Center at the UCLA Children's Discovery and Innovation Institute, Los Angeles, California, U.S.A.
Leah LeibovitchDepartment of Pediatrics, Division of Neonatology & Developmental Biology, Neonatal Research Center at the UCLA Children's Discovery and Innovation Institute, Los Angeles, California, U.S.A.
Sherin U DevaskarDepartment of Pediatrics, Division of Neonatology & Developmental Biology, Neonatal Research Center at the UCLA Children's Discovery and Innovation Institute, Los Angeles, California, U.S.A.
Brain Mapping Foundation · USInstitute for Molecular Medicine · US

Funding

UCLA Center for Translational Research in Neurodevelopment: UC-TRaNU54HD087101 · NICHD · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI MCCRACKEN, JAMES T. · 2016 to 2020
$6.5M
Prenatal Origins of Neurometabolic ConsequencesR01HD081206 · NICHD · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI DEVASKAR, SHERIN U · 2015 to 2024
$4.1M
NICHD NIH HHS R01 HD081206NICHD NIH HHS U54 HD087101
6 · The paper itself

Abstract

We tested the hypothesis that exposure of glut3+/- mice to a ketogenic diet ameliorates autism-like features, which include aberrant behavior and electrographic seizures. We first investigated the life course sex-specific changes in basal plasma-cerebrospinal fluid (CSF)-brain metabolic profile, brain glucose transport/uptake, glucose and monocarboxylate transporter proteins, and adenosine triphosphate (ATP) in the presence or absence of systemic insulin administration. Glut3+/- male but not female mice (5 months of age) displayed reduced CSF glucose/lactate concentrations with no change in brain Glut1, Mct2, glucose uptake or ATP. Exogenous insulin-induced hypoglycemia increased brain glucose uptake in glut3+/- males alone. Higher plasma-CSF ketones (β-hydroxybutyrate) and lower brain Glut3 in females vs males proved protective in the former while enhancing vulnerability in the latter. As a consequence, increased synaptic proteins (neuroligin4 and SAPAP1) with spontaneous excitatory postsynaptic activity subsequently reduced hippocampal glucose content and increased brain amyloid β1-40 deposition in an age-dependent manner in glut3+/- males but not females (4 to 24 months of age). We then explored the protective effect of a ketogenic diet on ultrasonic vocalization, sociability, spatial learning and memory, and electroencephalogram seizures in male mice (7 days to 6 to 8 months of age) alone. A ketogenic diet partially restored sociability without affecting perturbed vocalization, spatial learning and memory, and reduced seizure events. We conclude that (1) sex-specific and age-dependent perturbations underlie the phenotype of glut3+/- mice, and (2) a ketogenic diet ameliorates seizures caused by increased cortical excitation and improves sociability, but fails to rescue vocalization and cognitive deficits in glut3+/- male mice.

Indexed as

Diet, KetogenicSocial BehaviorAnimalsBehavior, AnimalBrainCell Adhesion Molecules, NeuronalElectroencephalographyFemaleGlucoseGlucose Transporter Type 3MaleMemoryMiceMice, KnockoutNerve Tissue ProteinsSeizuresCell Adhesion Molecules, NeuronalGlucoseGlucose Transporter Type 3Nerve Tissue ProteinsNlgn4 protein, mouse

Identifiers

PMID28324109
PMCPMC5460805
OpenAlexW2605146827

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.