Evidence map›Paper›PMID 39197039›Full record

ArticlePloS one2024

Knockout of the orphan membrane transporter Slc22a23 leads to a lean and hyperactive phenotype with a small hippocampal volume.

Yasuhiro Uchimura, Kodai Hino, Kosuke Hattori, Yoshinori Kubo, Airi Owada, Tomoko Kimura, Lucia Sugawara, Shinji Kume, Jean-Pierre Bellier, Daijiro Yanagisawa and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Pharmaceutics · 2026
    Article
  2. Alzheimer's disease multi-ancestry genome-wide interaction and stratified study with smoking.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  3. 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

15 authors.

Yasuhiro UchimuraDivision of Anatomy and Cell Biology, Department of Anatomy, Shiga University of Medical Science, Otsu, Shiga, Japan.ORCID 0000-0001-8633-2468
Kodai HinoDivision of Anatomy and Cell Biology, Department of Anatomy, Shiga University of Medical Science, Otsu, Shiga, Japan.
Kosuke HattoriDivision of Animal Genetics, Laboratory Animal Research Center, Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Yoshinori KuboDivision of Anatomy and Cell Biology, Department of Anatomy, Shiga University of Medical Science, Otsu, Shiga, Japan.
Airi OwadaDivision of Anatomy and Cell Biology, Department of Anatomy, Shiga University of Medical Science, Otsu, Shiga, Japan.
Tomoko KimuraDivision of Anatomy and Cell Biology, Department of Anatomy, Shiga University of Medical Science, Otsu, Shiga, Japan.
Lucia SugawaraDepartment of Medicine, Shiga University of Medical Science, Otsu, Shiga, Japan.
Shinji KumeDepartment of Medicine, Shiga University of Medical Science, Otsu, Shiga, Japan.
Jean-Pierre BellierMolecular Neuroscience Research Center, Shiga University of Medical Science, Otsu, Shiga, Japan.
Daijiro YanagisawaMolecular Neuroscience Research Center, Shiga University of Medical Science, Otsu, Shiga, Japan.
Akihiko ShiinoMolecular Neuroscience Research Center, Shiga University of Medical Science, Otsu, Shiga, Japan.
Takahisa NakayamaDivision of Human Pathology, Shiga University of Medical Science, Otsu, Shiga, Japan.
Yataro DaigoDepartment of Medical Oncology, Cancer Center and Center for Advanced Medicine against Cancer, Shiga University of Medical Science, Otsu, Shiga, Japan.
Tomoji MashimoDivision of Animal Genetics, Laboratory Animal Research Center, Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Jun UdagawaDivision of Anatomy and Cell Biology, Department of Anatomy, Shiga University of Medical Science, Otsu, Shiga, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epidemiological studies suggest that poor nutrition during pregnancy predisposes offspring to the development of lifestyle-related noncommunicable diseases and psychiatric disorders later in life. However, the molecular mechanisms underlying this predisposition are not well understood. In our previous study, using rats as model animals, we showed that behavioral impairments are induced by prenatal undernutrition. In this study, we identified solute carrier 22 family member 23 (Slc22a23) as a gene that is irreversibly upregulated in the rat brain by undernutrition during fetal development. Because the substrate of the SLC22A23 transporter has not yet been identified and the biological role of the Slc22a23 gene in vivo is not fully understood, we generated pan-Slc22a23 knockout rats and examined their phenotype in detail. The Slc22a23 knockout rats showed a lean phenotype, an increase in spontaneous locomotion, and improved endurance, indicating that they are not overweight and are even healthier in an ad libitum feeding environment. However, the knockout rats had reduced hippocampal volume, and the behavioral analysis suggested that they may have impaired cognitive function regarding novel objects.

Indexed as

HippocampusPhenotypeAnimalsBehavior, AnimalFemaleGene Knockout TechniquesLocomotionMalePregnancyRats

Identifiers

PMID39197039
PMCPMC11356391

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Registered trials

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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.