Evidence map›Paper›PMID 32703163›Full record

ArticleBMC genetics2020

Type 2 diabetes susceptibility genes on mouse chromosome 11 under high sucrose environment.

Misato Kobayashi, Hironori Ueda, Naru Babaya, Michiko Itoi-Babaya, Shinsuke Noso, Tomomi Fujisawa, Fumihiko Horio, Hiroshi Ikegami

Open access · diamondAbstract read
In one paragraph

Article in BMC genetics, 2020. 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
0.4field-weighted citation impact, top 37% 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

3 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
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

8 authors at 5 institutions in 1 country.

Misato KobayashiDepartment of Geriatric Medicine, Osaka University Graduate School of Medicine, Osaka, Japan.
Hironori UedaDepartment of Molecular Endocrinology, Osaka University Graduate School of Medicine, Osaka, Japan.
Naru BabayaDepartment of Endocrinology, Metabolism and Diabetes, Kindai University Faculty of Medicine, 337-2 Ohno-higashi, Osaka-sayama, Osaka, 589-8511, Japan.
Michiko Itoi-BabayaDepartment of Geriatric Medicine, Osaka University Graduate School of Medicine, Osaka, Japan.
Shinsuke NosoDepartment of Endocrinology, Metabolism and Diabetes, Kindai University Faculty of Medicine, 337-2 Ohno-higashi, Osaka-sayama, Osaka, 589-8511, Japan.
Tomomi FujisawaDepartment of Geriatric Medicine, Osaka University Graduate School of Medicine, Osaka, Japan.
Fumihiko HorioDepartment of Animal Sciences, Graduate School of Bioagricultural Sciences, Nagoya University, Nagoya, Japan.
Hiroshi IkegamiDepartment of Endocrinology, Metabolism and Diabetes, Kindai University Faculty of Medicine, 337-2 Ohno-higashi, Osaka-sayama, Osaka, 589-8511, Japan. ikegami@med.kindai.ac.jp.ORCID 0000-0001-8808-4605
Kindai University · JPNagoya University · JPKwansei Gakuin University · JPSakai Municipal Hospital · JPThe University of Osaka · JP

Funding

Research fellow of the Japan Society for the Promotion of Science 04J07821Scientific Research from the Ministry of Education, Science, Sports and Culture 15K09403Scientific Research from the Ministry of Education, Science, Sports and Culture 18K08493Scientific Research from the Ministry of Education, Science, Sports and Culture 24591346Scientific Research from the Ministry of Education, Science, Sports and Culture, Japan 16390264
6 · The paper itself

Abstract

backgroundBoth genetic and environmental factors contribute to type 2 diabetes development. We used consomic mice established from an animal type 2 diabetes model to identify susceptibility genes that contribute to type 2 diabetes development under specific environments. We previously established consomic strains (C3H-Chr 11

resultsIn C3H-Chr 11

conclusionsGenes on mouse Chr 11 could explain glucose intolerance, impaired insulin secretion, insulin resistance in NSY mice under sucrose administration. Congenic mapping with high sucrose environment localized susceptibility genes for type 2 diabetes associated with impaired insulin secretion in the middle segment (26.0-63.4 Mb) of Chr 11. Gene(s) that decrease white adipose tissue were mapped to the distal segment of Chr 11. The identification of diabetogenic gene on Chr 11 in the future study will facilitate precision medicine in type 2 diabetes by controlling specific environments in targeted subjects with susceptible genotypes.

Indexed as

Genetic Predisposition to DiseaseAnimalsChromosome MappingDiabetes Mellitus, Type 2Disease Models, AnimalHyperglycemiaInsulinInsulin ResistanceMaleMiceMice, CongenicMice, Inbred C3HPhenotypeSucroseInsulinSucroseCongenic strainConsomic strainInsulin resistanceInsulin secretionNSY miceSucroseSusceptibility geneType 2 diabetes

Identifiers

PMID32703163
PMCPMC7379357
OpenAlexW3044539736

What OpenQuestion holds

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LicenceCC BY
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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.