Evidence map›Paper›PMID 39134590›Full record

ArticleScientific reports2024

Disruption of insulin receptor substrate 2 (IRS2) causes non-obese type 2 diabetes with β-cell dysfunction in the golden (Syrian) hamster.

Michiko Hirose, Kimiko Inoue, Shogo Matoba, Takaki Tatebe, Syun Tokita, Yukiko Dodo, Toshiko Tomishima, Ayumi Hasegawa, Arata Honda, Mao Ozaki and 7 more

Abstract read
In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Review
  2. Article
  3. A simplified protocol for vitrification of hamster embryos.The Journal of reproduction and development · 2025
    Article
  4. 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

17 authors.

Michiko HiroseRIKEN BioResource Research Center, Ibaraki, Japan.
Kimiko InoueRIKEN BioResource Research Center, Ibaraki, Japan.
Shogo MatobaRIKEN BioResource Research Center, Ibaraki, Japan.
Takaki TatebeRIKEN BioResource Research Center, Ibaraki, Japan.
Syun TokitaRIKEN BioResource Research Center, Ibaraki, Japan.
Yukiko DodoRIKEN BioResource Research Center, Ibaraki, Japan.
Toshiko TomishimaRIKEN BioResource Research Center, Ibaraki, Japan.
Ayumi HasegawaRIKEN BioResource Research Center, Ibaraki, Japan.
Arata HondaCenter for Development of Advanced Medical Technology, Jichi Medical University School of Medicine, Tochigi, Japan.
Mao OzakiRIKEN BioResource Research Center, Ibaraki, Japan.
Akiko ShinogiRIKEN BioResource Research Center, Ibaraki, Japan.
Ryoko YanagisawaRIKEN BioResource Research Center, Ibaraki, Japan.
Muhammad FauziDepartment of Diabetes, Endocrinology and Nutrition, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Takaaki MurakamiDepartment of Diabetes, Endocrinology and Nutrition, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Nobuya InagakiDepartment of Diabetes, Endocrinology and Nutrition, Graduate School of Medicine, Kyoto University, Kyoto, Japan. inagaki@kuhp.kyoto-u.ac.jp.
Masaru TamuraRIKEN BioResource Research Center, Ibaraki, Japan. masaru.tamura@riken.jp.
Atsuo OguraRIKEN BioResource Research Center, Ibaraki, Japan. ogura@rtc.riken.go.jp.

Funding

Grants-in-Aid for Scientific Research (KAKENHI) from the Japan Society for the Promotion of Science 23H04956Grants-in-Aid for Scientific Research (KAKENHI) from the Japan Society for the Promotion of Science JP19H03151
6 · The paper itself

Abstract

Because of the advent of genome-editing technology, gene knockout (KO) hamsters have become attractive research models for diverse diseases in humans. This study established a new KO model of diabetes by disrupting the insulin receptor substrate-2 (Irs2) gene in the golden (Syrian) hamster. Homozygous KO animals were born alive but with delayed postnatal growth until adulthood. They showed hyperglycemia, high HbA1c, and impaired glucose tolerance. However, they normally responded to insulin stimulation, unlike Irs2 KO mice, an obese type 2 diabetes (T2D) model. Consistent with this, Irs2 KO hamsters did not increase serum insulin levels upon glucose administration and showed β-cell hypoplasia in their pancreas. Thus, our Irs2 KO hamster provide a unique T2D animal model that is distinct from the obese T2D models. This model may contribute to a better understanding of the pathophysiology of human non-obese T2D with β-cell dysfunction, the most common type of T2D in East Asian countries, including Japan.

Indexed as

Diabetes Mellitus, Type 2Insulin Receptor Substrate ProteinsMesocricetusAnimalsBlood GlucoseCricetinaeDisease Models, AnimalGene Knockout TechniquesHumansInsulinInsulin-Secreting CellsMaleBlood GlucoseInsulinInsulin Receptor Substrate ProteinsAnimal modelGlucose metabolismInsulinPancreasType 2 diabetes mellitus

Identifiers

PMID39134590
PMCPMC11319448

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.