2026-10-11T21:18:28Z https://api.figshare.com/v2/oai

oai:figshare.com:article/33817014 2026-09-15T18:22:53Z category_4 category_12 category_15 category_873 category_106 category_811 category_64 portal_5 item_type_3 month_year_09_2026

pcbi.1014589.t002 - <p> </p> Aurore Woller (5093966) Yuval Tamir (16499028) Alon Bar (9994739) Avi Mayo (181415) Michal Rein (4633807) Anastasia Godneva (10341142) Netta Mendelson Cohen (24951303) Eran Segal (26774) Yoel Toledano (354161) Smadar Shilo (10993386) Didier Gonze (69567) Uri Alon (15569) Biochemistry Cell Biology Neuroscience Chemical Sciences not elsewhere classified Science Policy Mathematical Sciences not elsewhere classified Cancer maximum compensation level beta cell function xlink "> prediabetes understudied risk factor enhanced insulin secretion control blood glucose cell carrying capacity carrying capacity relies beta cell compensation unlike insulin resistance low carrying capacity prediabetes </ p estimated using homa carrying capacity quantified using insulin resistance beta cells low homa year follow uses prediabetes subclinical state secreted insulin prediabetic people needed amount measured glucose mathematical model many individuals insulin measurements insulin levels individuals seem higher risk high glucose fold variation finding 10 experimental testing better understand b formula <div><p>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.</p></div> 2026-09-15T18:01:12Z Dataset Dataset 10.1371/journal.pcbi.1014589.t002 https://figshare.com/articles/dataset/pcbi_1014589_t002_-_p_p_/33817014 CC BY 4.0