Evidence map›Paper›PMID 40509916›Full record

ArticleDiabetes care2025

Rapid and Slow Progressors Toward β-Cell Depletion and Their Predictors in Type 1 Diabetes: Prospective Longitudinal Study in Japanese Type 1 Diabetes (TIDE-J).

Shinsuke Noso, Daisuke Chujo, Akihisa Imagawa, Eiji Kawasaki, Takuya Awata, Kazuki Yasuda, Norio Abiru, Noriko Kodani, Yoichi Oikawa, Tomoyasu Fukui and 15 more

Abstract readMulticenter Study
In one paragraph

Article in Diabetes care, 2025. 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
–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

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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.

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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

25 authors.

Shinsuke NosoDepartment of Endocrinology, Metabolism and Diabetes, Kindai University Faculty of Medicine, Osaka-Sayama, Osaka, Japan.ORCID 0000-0002-0943-8450
Daisuke ChujoDepartment of Diabetes, Metabolism, and Endocrinology, International University of Health and Welfare, Ichikawa, Japan.ORCID 0000-0001-7727-6310
Akihisa ImagawaDepartment of Internal Medicine (I), Osaka Medical and Pharmaceutical University, Takatsuki, Japan.ORCID 0000-0002-4213-3229
Eiji KawasakiDiabetes, Thyroid and Endocrine Center, Shin-Koga Hospital, Kurume, Japan.ORCID 0000-0001-7434-4744
Takuya AwataOkinaka Memorial Institute for Medical Research, Tokyo, Japan.ORCID 0000-0003-2622-8129
Kazuki YasudaDepartment of Diabetes, Endocrinology, and Metabolism, Kyorin University, Mitaka, Japan.ORCID 0000-0002-6966-496X
Norio AbiruDepartment of Endocrinology and Metabolism, Nagasaki University Graduate School of Biomedical Science, Nagasaki, Japan.
Noriko KodaniDepartment of Diabetes, Endocrinology, and Metabolism, National Center for Global Health and Medicine, Japan Institute for Health Security, Tokyo, Japan.ORCID 0000-0002-4443-1545
Yoichi OikawaDepartment of Endocrinology and Diabetes, School of Medicine, Saitama Medical University, Iruma, Japan.ORCID 0000-0003-1524-6751
Tomoyasu FukuiDivision of Diabetes and Endocrinology, Showa University School of Medicine, Tokyo, Japan.ORCID 0000-0002-8535-008X
Takeshi KatsukiDepartment of Diabetes and Endocrinology, Tokyo Saiseikai Central Hospital, Tokyo, Japan.
Junji KozawaDepartment of Metabolic Medicine, Graduate School of Medicine, Osaka University, Suita, Japan.ORCID 0000-0001-9665-8947
Kan NagasawaDivision of Diabetes, Metabolism, and Endocrine Medicine Field, Iwate Medical University, Shiwa, Japan.
Haruhiko OsawaDepartment of Diabetes and Molecular Genetics, Ehime University Graduate School of Medicine, Toon, Japan.ORCID 0000-0003-0289-8363
Kazuma TakahashiIwate Prefectural University, Takizawa, Japan.
Kyoichiro TsuchiyaDepartment of Diabetes and Endocrinology, University of Yamanashi Hospital, Yamanashi, Japan.
Masayuki ShimodaDepartment of Pancreatic Islet Cell Transplantation, National Center for Global Health and Medicine, Japan Institute for Health Security, Tokyo, Japan.
Hisafumi YasudaDivision of Health Sciences, Department of Public Health, Kobe University Graduate School of Health Sciences, Kobe, Japan.ORCID 0000-0003-3742-9268
Norikazu MaedaDepartment of Endocrinology, Metabolism and Diabetes, Kindai University Faculty of Medicine, Osaka-Sayama, Osaka, Japan.ORCID 0000-0002-7105-0836
Akira ShimadaDepartment of Endocrinology and Diabetes, School of Medicine, Saitama Medical University, Iruma, Japan.ORCID 0000-0002-3954-4983
Tetsuro KobayashiOkinaka Memorial Institute for Medical Research, Tokyo, Japan.ORCID 0000-0002-4364-2527
Toshiaki HanafusaSakai City Medical Center, Sakai, Japan.ORCID 0000-0001-7482-6823
Hiroshi KajioDepartment of Diabetes, Endocrinology, and Metabolism, National Center for Global Health and Medicine, Japan Institute for Health Security, Tokyo, Japan.ORCID 0000-0002-5404-651X
Hiroshi IkegamiDepartment of Endocrinology, Metabolism and Diabetes, Kindai University Faculty of Medicine, Osaka-Sayama, Osaka, Japan.ORCID 0000-0001-8808-4605
Japanese Type 1 Diabetes Database Study (TIDE-J) Genetics

Funding

National Center for Global Health and Medicine 19A1008
6 · The paper itself

Abstract

objectiveThis study aimed to investigate the progression of β-cell dysfunction and its predictors in Japanese patients with type 1 diabetes, using data from the nationwide, multicenter, prospective longitudinal Japanese Type 1 Diabetes Database Study (TIDE-J). RESEARCH DESIGN AND

methodsTIDE-J enrolled 314 Japanese individuals with type 1 diabetes, including 165 with acute-onset, 105 with slowly progressive, and 44 with fulminant type 1 diabetes. Clinical data, including C-peptide levels, glycemic control, and autoantibody status, were collected annually for up to 14 years. HLA genotypes were analyzed at study entry. The time to insulin depletion was analyzed using survival curves and Cox proportional hazards models to determine predictive factors.

resultsThe rate of undetectable C-peptide varied significantly among subtypes. At 5 years after onset, 43.1% (n = 55) of patients with acute-onset, 9.1% (n = 7) with slowly progressive, and 93.2% (n = 38) with fulminant type 1 diabetes reached undetectable C-peptide. Even within acute-onset type 1 diabetes, a marked interindividual variation was observed in the progression toward β-cell depletion. HLA genotypes influenced progression rates as follows: DRB1*04:05-DQB1*04:01/DRB1*04:05-DQB1*04:01 (DR4/DR4) carriers exhibited slower β-cell depletion, whereas DR4/DRB1*08:02-DQB1*03:02 (i.e., DR4/DR8) and DR4/DRB1*09:01-DQB1*03:03 (i.e., DR4/DR9) were associated with a rapid progression. For slowly progressive type 1 diabetes, low BMI, GAD antibody positivity, and absence of the DRB1*15:01-DQB1*06:02 or DRB1*15:02-DQB1*06:01 (i.e., DR2) haplotype were predictive of progression to insulin dependence.

conclusionsThis study elucidates the heterogeneity in β-cell dysfunction among Japanese individuals with type 1 diabetes and identifies genetic and clinical predictors of disease progression. These findings provide insights for individualized management strategies and future therapeutic interventions.

Indexed as

Diabetes Mellitus, Type 1Insulin-Secreting CellsAdolescentAdultAutoantibodiesChildChild, PreschoolC-PeptideDisease ProgressionEast Asian PeopleFemaleGenotypeHumansJapanLongitudinal StudiesMaleAutoantibodiesC-Peptide

Identifiers

PMID40509916
PMCPMC12281979

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