Evidence map›Paper›PMID 30970177›Full record

ArticleJournal of diabetes investigation2019

Variants in the BACH2 and CLEC16A gene might be associated with susceptibility to insulin-triggered type 1 diabetes.

Hiroshi Onuma, Ryoichi Kawamura, Yasuharu Tabara, Masakatsu Yamashita, Jun Ohashi, Eiji Kawasaki, Akihisa Imagawa, Yuya Yamada, Daisuke Chujo, Kenji Takahashi and 4 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
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 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

9 citing papers in PubMed, 11 citations in OpenAlex.

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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

14 authors at 11 institutions in 1 country.

Hiroshi OnumaDepartment of Diabetes and Molecular Genetics, Ehime University Graduate School of Medicine, To-on, Ehime, Japan.ORCID https://orcid.org/0000-0002-6595-7677
Ryoichi KawamuraDepartment of Diabetes and Molecular Genetics, Ehime University Graduate School of Medicine, To-on, Ehime, Japan.
Yasuharu TabaraCenter for Genomic Medicine, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Masakatsu YamashitaDepartment of Immunology, Ehime University Graduate School of Medicine, To-on, Ehime, Japan.
Jun OhashiDepartment of Biological Sciences, Graduate School of Science, The University of Tokyo, Tokyo, Japan.
Eiji KawasakiDepartment of Diabetes and Endocrinology, Shin-Koga Hospital, Kurume, Fukuoka, Japan.ORCID https://orcid.org/0000-0001-7434-4744
Akihisa ImagawaDepartment of Internal Medicine (I), Osaka Medical College, Takatsuki, Osaka, Japan.
Yuya YamadaDepartment of Endocrinology and Metabolism, Sumitomo Hospital, Osaka, Japan.
Daisuke ChujoDepartment of Diabetes, Endocrinology and Metabolism, National Center for Global Health and Medicine, Tokyo, Japan.ORCID https://orcid.org/0000-0001-7727-6310
Kenji TakahashiDepartment of Internal Medicine, Diabetes Division, Kurashiki Central Hospital, Kurashiki, Okayama, Japan.
Tadashi SuehiroDepartment of Diabetes, Kochi Takasu Hospital, Kochi, Kochi, Japan.
Yasunori TakataDepartment of Diabetes and Molecular Genetics, Ehime University Graduate School of Medicine, To-on, Ehime, Japan.
Haruhiko OsawaDepartment of Diabetes and Molecular Genetics, Ehime University Graduate School of Medicine, To-on, Ehime, Japan.
Hideichi MakinoDepartment of Diabetes and Molecular Genetics, Ehime University Graduate School of Medicine, To-on, Ehime, Japan.
Ehime University · JPEhime Medical Center · JPKoga Hospital · JPKurashiki Central Hospital · JPKyoto University · JPNational Center for Global Health and Medicine · JPOsaka Medical and Pharmaceutical University · JPSanraku Hospital · JPSumitomo Hospital · JPThe University of Tokyo · JPTokyo Women's Medical University · JP

Funding

Diawa Securities Health FoundationEhime UniversityMr. Takashi IkedaNOVARTIS Foundation (Japan) for the Promotion of ScienceTakeda Science FoundationUehara Memorial Foundation
6 · The paper itself

Abstract

AIM/

introductionInsulin administration was found to trigger type 1 diabetes in six Japanese type 2 diabetes patients with type 1 diabetes high-risk human leukocyte antigen class II and the class I allele of the insulin gene variable number tandem repeat genotype. The objective of the present study was to assess the contribution of non-human leukocyte antigen single-nucleotide polymorphisms (SNPs) to the risk of developing insulin-triggered type 1 diabetes. MATERIALS AND

methodsWe genotyped 13 type 1 diabetes susceptible SNPs in six patients and compared them with those in Japanese controls (Hap Map3-JPT). The SNPs that showed statistically significant results were further analyzed using non-diabetic control participants and participants with type 2 diabetes at the Ehime University Hospital.

resultsThe risk allele frequency of BACH2 rs3757247 in the six patients was significantly more frequent than that in 86 Japanese controls (P = 0.038). No significant difference in the allele frequency was observed in the other SNPs. This result was confirmed by the findings that the risk allele frequency of BACH2 in the six patients was significantly higher than that in the non-diabetic control participants (n = 179) and type 2 diabetes with or without insulin treatment (n = 154 or n = 152; P = 0.035, 0.034 or 0.037, respectively). Despite being statistically not significant, the six patients were all homozygous for the CLEC16A rs12708716 risk allele and five were homozygous for the CLEC16A rs2903692 risk allele.

conclusionsIn addition to type 1 diabetes high-risk human leukocyte antigen class II and the class I allele of the insulin gene variable number tandem repeat genotype, the possibility that the risk variants of BACH2 and CLEC16A could contribute to the development of insulin-triggered type 1 diabetes cannot be excluded.

Indexed as

Genetic Predisposition to DiseasePolymorphism, Single NucleotideBasic-Leucine Zipper Transcription FactorsBiomarkersCase-Control StudiesDiabetes Mellitus, Type 1FemaleFollow-Up StudiesGenotypeHumansInsulinLectins, C-TypeMaleMiddle AgedMonosaccharide Transport ProteinsPrognosisBACH2 protein, humanBasic-Leucine Zipper Transcription FactorsBiomarkersCLEC16A protein, humanInsulinLectins, C-TypeMonosaccharide Transport ProteinsBACH2CLEC16AInsulin-triggered type 1 diabetes

Identifiers

PMID30970177
PMCPMC6825945
OpenAlexW2937588180

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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.