Evidence map›Paper›PMID 42743393›Full record

ArticlePLoS computational biology2026

Quantification of beta-cell carrying capacity in prediabetes.

Aurore Woller, Yuval Tamir, Alon Bar, Avi Mayo, Michal Rein, Anastasia Godneva, Netta Mendelson Cohen, Eran Segal, Yoel Toledano, Smadar Shilo and 2 more

Abstract read
In one paragraph

Article in PLoS computational biology, 2026. 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

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.

  1. Article
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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

12 authors.

Aurore WollerDepartment of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel.
Yuval TamirDepartment of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel.
Alon BarDepartment of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel.
Avi MayoDepartment of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel.ORCID https://orcid.org/0000-0002-4479-3423
Michal ReinDepartment of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel.
Anastasia GodnevaDepartment of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel.
Netta Mendelson CohenDepartment of Computer Sciences and Applied Mathematics, Weizmann Institute of Science, Rehovot, Israel.
Eran SegalDepartment of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel.
Yoel ToledanoDivision of Maternal Fetal Medicine, Helen Schneider Women's Hospital, Rabin Medical Center, Petah Tikva, Israel.
Smadar ShiloDepartment of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel.
Didier GonzeUnité de Chronobiologie théorique, Faculté des Sciences, Université Libre de Bruxelles (ULB), Brussels, Belgium.
Uri AlonDepartment of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prediabetes, a subclinical state of high glucose, carries a risk of transitioning to diabetes. One cause of prediabetes is insulin resistance, which impairs the ability of insulin to control blood glucose. However, many individuals with high insulin resistance retain normal glucose due to compensation by enhanced insulin secretion by beta cells. Individuals seem to differ in their maximum compensation level, termed beta cell carrying capacity, such that low carrying capacity is associated with a higher risk of prediabetes and diabetes. Carrying capacity has not been quantified using a mathematical model and at present cannot be estimated from measured glucose and insulin levels in patients, unlike insulin resistance and beta cell function which can be estimated using HOMA-IR and HOMA-B formula. Here we present a mathematical model of beta cell compensation and carrying capacity, and develop a new formula called HOMA-C to estimate it from glucose and insulin measurements. HOMA-C estimates the maximal potential beta cell function of an individual, rather than the current beta cell function. It uses prediabetes as a stress and estimates carrying capacity using the gap between secreted insulin and the needed amount of insulin for homeostasis. We test this approach using longitudinal cohorts of prediabetic people, finding 10-fold variation in carrying capacity. Low HOMA-C associates with higher risk of transitioning to diabetes in a one-year follow up. The interpretation of HOMA-C as a carrying capacity relies on a mathematical model and requires further experimental testing. Quantification of beta cell carrying capacity may help to better understand this understudied risk factor for diabetes.

Indexed as

Insulin-Secreting CellsModels, BiologicalPrediabetic StateBlood GlucoseHumansInsulinInsulin ResistanceBlood GlucoseInsulin

Identifiers

PMID42743393
PMCPMC13638054

What OpenQuestion holds

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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.