Evidence map›Paper›PMID 32699230›Full record

ArticleScientific reports2020

Insulin2

Daisuke Sakano, Airi Inoue, Takayuki Enomoto, Mai Imasaka, Seiji Okada, Mutsumi Yokota, Masato Koike, Kimi Araki, Shoen Kume

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.8field-weighted citation impact, top 27% 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

5 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. How can we establish animal models of HIV-associated lymphoma?Animal models and experimental medicine · 2024
    Review
  3. Review
  4. Article
  5. 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

9 authors at 4 institutions in 1 country.

Daisuke Sakano *School of Life Science and Technology, Tokyo Institute of Technology, 4259-B-25 Nagatsuta-cho, Midori-ku, Yokohama, Kanagawa, 226-8501, Japan.
Airi Inoue *School of Life Science and Technology, Tokyo Institute of Technology, 4259-B-25 Nagatsuta-cho, Midori-ku, Yokohama, Kanagawa, 226-8501, Japan.
Takayuki EnomotoSchool of Life Science and Technology, Tokyo Institute of Technology, 4259-B-25 Nagatsuta-cho, Midori-ku, Yokohama, Kanagawa, 226-8501, Japan.
Mai ImasakaLaboratory of Developmental Genetics, Institute of Resource Development and Analysis, Chuo-Ku, Honjo 2-2-1, Kumamoto, 860-0811, Japan.
Seiji OkadaDivision of Hematopoiesis, Joint Research Center for Retroviral Infection, Kumamoto University, Honjo 2-2-1, Kumamoto, 860-0811, Japan.ORCID http://orcid.org/0000-0003-3124-5206
Mutsumi YokotaDepartment of Cell Biology and Neuroscience, Juntendo University Graduate School of Medicine, Hongo 2-1-1, Bunkyo-ku, Tokyo, 113-8421, Japan.
Masato KoikeDepartment of Cell Biology and Neuroscience, Juntendo University Graduate School of Medicine, Hongo 2-1-1, Bunkyo-ku, Tokyo, 113-8421, Japan.ORCID http://orcid.org/0000-0002-3174-5684
Kimi ArakiLaboratory of Developmental Genetics, Institute of Resource Development and Analysis, Chuo-Ku, Honjo 2-2-1, Kumamoto, 860-0811, Japan. arakimi@gpo.kumamoto-u.ac.jp.
Shoen KumeSchool of Life Science and Technology, Tokyo Institute of Technology, 4259-B-25 Nagatsuta-cho, Midori-ku, Yokohama, Kanagawa, 226-8501, Japan. skume@bio.titech.ac.jp.
Tokyo Institute of Technology · JPJuntendo University · JPKumamoto University · JPHyogo Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Insulin gene mutations have been identified to cause monogenic diabetes, and most of which developed permanent neonatal diabetes at young ages before 6 months of age in humans. To establish an animal model of permanent diabetes, we performed genome editing using the CRISPR/Cas9 system. We generated a novel Kuma mutant mice with p.Q104del in the Insulin2 (Ins2) gene in a BRJ background that exhibits a severe immune deficiency. Kuma mutant mice are non-obese and developed hyperglycemia from 3 weeks after birth in both males and females, which are inherited in a dominant mode. Kuma mutant mice displayed reduced insulin protein levels from 3-weeks-old, which seem to be caused by the low stability of the mutant insulin protein. Kuma mutant showed a reduction in islet size and islet mass. Electron microscopic analysis revealed a marked decrease in the number and size of insulin granules in the beta-cells of the mutant mice. Hyperglycemia of the mutant can be rescued by insulin administration. Our results present a novel insulin mutation that causes permanent early-onset diabetes, which provides a model useful for islet transplantation studies.

Indexed as

AnimalsCRISPR-Cas SystemsDisease Models, AnimalEndoplasmic Reticulum StressFemaleGene EditingGlucose Tolerance TestHyperglycemiaInsulinInsulin-Secreting CellsIslets of LangerhansMaleMiceMice, Inbred BALB CMice, KnockoutMicroscopy, ElectronInsulinOligodeoxyribonucleotides

Identifiers

PMID32699230
PMCPMC7376009
OpenAlexW3045178656

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.