Evidence map›Paper›PMID 29987871›Full record

ArticleJournal of diabetes investigation2019

Novel murine model of congenital diabetes: The insulin hyposecretion mouse.

Kenta Nakano, Rieko Yanobu-Takanashi, Yuki Takahashi, Hayato Sasaki, Yukiko Shimizu, Tadashi Okamura, Nobuya Sasaki

Open access · goldAbstract read
In one paragraph

Article in Journal of diabetes investigation, 2019. 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
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

4 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. A deletion in the Ctns gene causes renal tubular dysfunction and cystine accumulation in LEA/Tohm rats.Mammalian genome : official journal of the International Mammalian Genome Society · 2019
    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

7 authors at 2 institutions in 1 country.

Kenta NakanoLaboratory of Laboratory Animal Science and Medicine, School of Veterinary Medicine, Kitasato University, Towada, Japan.
Rieko Yanobu-TakanashiDepartment of Laboratory Animal Medicine, Research Institute, National Center for Global Health and Medicine (NCGM), Tokyo, Japan.
Yuki TakahashiLaboratory of Laboratory Animal Science and Medicine, School of Veterinary Medicine, Kitasato University, Towada, Japan.
Hayato SasakiLaboratory of Laboratory Animal Science and Medicine, School of Veterinary Medicine, Kitasato University, Towada, Japan.
Yukiko ShimizuDepartment of Laboratory Animal Medicine, Research Institute, National Center for Global Health and Medicine (NCGM), Tokyo, Japan.
Tadashi OkamuraDepartment of Laboratory Animal Medicine, Research Institute, National Center for Global Health and Medicine (NCGM), Tokyo, Japan.
Nobuya SasakiLaboratory of Laboratory Animal Science and Medicine, School of Veterinary Medicine, Kitasato University, Towada, Japan.ORCID http://orcid.org/0000-0002-7971-3024
National Center for Global Health and Medicine · JPKitasato University · JP

Funding

Grants-in-Aid for Research from the National Center for Global Health and Medicine 26-105 and 29-1001Grants-in-Aid for Scientific Research, KAKENHI 16K07094 and 26430101Ministry of Education, Culture, Sports, Science and Technology (MEXT)
6 · The paper itself

Abstract

AIMS/

introductionDiabetic animal models have made an enormous contribution to our understanding of the etiology of diabetes and the development of new medications. The aim of the present study was to develop and characterize a novel, non-obese murine strain with spontaneous diabetes - the insulin hyposecretion (ihs) mouse. MATERIALS AND

methodsDuring the development of the ICGN.B6-Tns2

resultsThe ihs mice showed several distinctive diabetes-related characteristics: (i) the onset of diabetes was observed only in the male mice; (ii) there were no differences in insulin content between the ihs and control mice; (iii) impaired insulin secretion was elicited by glucose, potassium chloride and sulfonylureas; (iv) there was a significant reduction of relative β-cell volume with no signs of inflammation or fibrosis; (v) they showed a normal glycemic response to exogenous insulin; and (vi) the mice were not obese.

conclusionsThe ihs mouse provides a novel murine model of congenital diabetes that shows insulin secretion failure. This model allows not only an analysis of the progression of diabetes, but also the identification of unknown genes involved in insulin secretion.

Indexed as

Insulin SecretionAnimalsBlood GlucoseDiabetes Mellitus, ExperimentalFemaleInsulin-Secreting CellsMaleMiceMice, Inbred C57BLMice, Inbred ICRTensinsBlood GlucoseTensinsTns2 protein, mouseHyperglycemiaHypoinsulinemiaNon-obese diabetic mouse

Identifiers

PMID29987871
PMCPMC6400215
OpenAlexW2813643876

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.