Evidence map›Paper›PMID 41554905›Full record

ArticleScientific reports2026

Revisiting type 1 diabetes progression in the non-obese diabetic mouse.

Barbara Ehall, Laurin Herbsthofer, Beate Obermüller, Ceren Karacay, Kaddour Bounab, Joakim Franz, Amin El-Heliebi, Beate Boulgaropoulos, Lilli Bonstingl, Katja Sallinger and 7 more

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In one paragraph

Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

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

1 citing paper in PubMed.

  1. 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

17 authors.

Barbara EhallDivision of Endocrinology and Diabetology, Department of Internal Medicine, Medical University of Graz, Graz, Austria.
Laurin HerbsthoferCenter for Biomarker Research in Medicine (CBmed) GmbH, Graz, Austria.
Beate ObermüllerDepartment of Paediatric and Adolescent Surgery, Medical University of Graz, Graz, Austria.
Ceren KaracayDivision of Endocrinology and Diabetology, Department of Internal Medicine, Medical University of Graz, Graz, Austria.
Kaddour BounabDivision of Endocrinology and Diabetology, Department of Internal Medicine, Medical University of Graz, Graz, Austria.
Joakim FranzDivision of Endocrinology and Diabetology, Department of Internal Medicine, Medical University of Graz, Graz, Austria.
Amin El-HeliebiDivision of Cell Biology, Histology and Embryology, Medical University of Graz, Graz, Austria.
Beate BoulgaropoulosDivision of Endocrinology and Diabetology, Department of Internal Medicine, Medical University of Graz, Graz, Austria.
Lilli BonstinglDivision of Cell Biology, Histology and Embryology, Medical University of Graz, Graz, Austria.
Katja SallingerDivision of Cell Biology, Histology and Embryology, Medical University of Graz, Graz, Austria.
Victoria HoisDivision of Endocrinology and Diabetology, Department of Internal Medicine, Medical University of Graz, Graz, Austria.
Clemens HarerDivision of Endocrinology and Diabetology, Department of Internal Medicine, Medical University of Graz, Graz, Austria.
Petra KotzbeckCOREMED -Centre for Regenerative and Precision Medicine, Joanneum Research Forschungsgesellschaft mbH, Graz, Austria.
Wolfgang F GraierDivision of Molecular Biology and Biochemistry, Gottfried Schatz Research Center for Cellular Signaling, Metabolism and Aging, Medical University of Graz, Graz, Austria.
Gabriele SchoiswohlDivision of Molecular Biology and Biochemistry, Gottfried Schatz Research Center for Cellular Signaling, Metabolism and Aging, Medical University of Graz, Graz, Austria.
Barbara PrietlDivision of Endocrinology and Diabetology, Department of Internal Medicine, Medical University of Graz, Graz, Austria.
Thomas R PieberDivision of Endocrinology and Diabetology, Department of Internal Medicine, Medical University of Graz, Graz, Austria. thomas.pieber@medunigraz.at.

Funding

BioTechMed-Graz Flagship Project 2020BioTechMed-Graz, Austria Flagship Project 2020
6 · The paper itself

Abstract

As conventional diagnostic criteria in non-obese diabetic (NOD) mice may not reflect the early phase of type 1 diabetes, the applicability of NOD mouse models for early type 1 diabetes in humans can be limited. We therefore aimed to assess stages of beta cell loss in early type 1 diabetes at blood glucose (BG) levels of 80–200 mg/dl in age-stratified NOD mice. Islet composition of five pancreas sections each from 38 female NOD mice was determined using multiplexed-immunohistochemistry staining and Cell2Grid/rule-based automated islet identification. Visual analysis of fm-IHC images led to classification of islet stages. Average islet stage per animal (Islet Score) was correlated with average BG to identify NOD mice subgroups of disease progression. We categorized 3324 islets into islet stages, describing beta cell loss from 0 to 4.The proportion of insulin-deficient islets increased from BG > 126 mg/dl onwards. Three disease progression subgroups in NOD mice were identified: Non-diabetic (Islet Score < 1.0, BG < 126 mg/dl), pre-diabetic (Islet Score > 1.0, BG < 126 mg/dl) and early-diabetic (Islet Score > 1.0, BG > 126 mg/dl and diabetes progression model was established. The revised classification of type 1 diabetes in NOD mice and the resulting type 1 diabetes progression model improves adaptation of the NOD model to human pathophysiology.

Indexed as

Diabetes Mellitus, Type 1AnimalsBlood GlucoseDisease Models, AnimalDisease ProgressionFemaleInsulinInsulin-Secreting CellsIslets of LangerhansMiceMice, Inbred NODBlood GlucoseInsulinBeta cell lossDiabetes thresholdDisease stagesEarly type 1 diabetesInsulitisIsletsNOD mouseStagesType 1 diabetes

Identifiers

PMID41554905
PMCPMC12894909

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Registered trials

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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.