# Validation of a Diabetes Subtype Classification Model Using Data from U.S. Adults Before and After the COVID-19 Pandemic

**Authors:** Brian Lu, Peng Li, Andrew B. Crouse, Tiffany Grimes, Ava N. Smith, Matthew Might, Fernando Ovalle, Anath Shalev

PMC · DOI: 10.3390/metabo16030204 · Metabolites · 2026-03-19

## TL;DR

This study validates a model for classifying diabetes subtypes and finds that severe diabetes subtypes increased after the pandemic.

## Contribution

A validated diabetes subtype classification model and evidence of changing subtype distribution post-pandemic.

## Key findings

- The model achieved 98% specificity and 93% sensitivity in classifying diabetes subtypes.
- Severe insulin-dependent diabetes increased from 42% to 61% at UAB post-pandemic.
- Similar increases in severe diabetes subtypes were observed in NHANES data.

## Abstract

Background: We (and others) have previously identified five clinically distinct diabetes subtypes. Currently, few models to identify diabetes subtypes are readily accessible. Further, while COVID-19 has been associated with increased risk of new-onset diabetes, it remains unknown whether the pandemic is also associated with changes in diabetes subtype distribution. Methods: We used the electronic health records of patients diagnosed with diabetes from 2010 to 2019 at the Kirklin Clinic of the University of Alabama at Birmingham (UAB) to train models to assign diabetes subtypes previously identified by hierarchical clustering. We then applied the trained model to conduct a retrospective cluster analysis of electronic health records of patients diagnosed with diabetes from 2020 to 2024 at UAB. We further validated our findings using data from the 2015–2023 National Health and Nutrition Examination Surveys (NHANES). Results: The trained classification model had an average specificity of 98% and an average sensitivity of 93%. Using the model, we identified a significant difference in the distribution of type 2 diabetes subtypes in patients at UAB and in participants in NHANES. In particular, the proportion of patients with severe insulin-dependent diabetes or severe insulin-resistant diabetes subtypes increased from 42% to 61% and 31% to 40% at the UAB and in NHANES, respectively. Conclusions: The model presented here can facilitate the identification of diabetes subtypes. The proportions of patients with severe subtypes of diabetes have seemed to increase in the more recent years following the pandemic. Further studies are required to determine the potential causes of this phenomenon.

## Linked entities

- **Diseases:** diabetes (MONDO:0005015), type 2 diabetes (MONDO:0005148)

## Full-text entities

- **Genes:** GAD1 (glutamate decarboxylase 1) [NCBI Gene 2571] {aka CPSQ1, DEE89, GAD, GAD-67, SCP}, GLUL (glutamate-ammonia ligase) [NCBI Gene 2752] {aka DEE116, GLNS, GS, PIG43, PIG59}, SLC5A2 (solute carrier family 5 member 2) [NCBI Gene 6524] {aka SGLT2}, INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}, GLP1R (glucagon like peptide 1 receptor) [NCBI Gene 2740] {aka GLP-1, GLP-1-R, GLP-1R}
- **Diseases:** insulin deficiency (MESH:D007333), infection (MESH:D007239), injury to (MESH:D014947), type 2 diabetes (MESH:D003924), obesity-related diabetes (MESH:D009765), heart or kidney disease (MESH:D007674), LADA (MESH:D000071698), age-related diabetes (MESH:D048909), diabetic neuropathy (MESH:D003929), T1D (MESH:D003922), MARD (MESH:C565101), cardiovascular complications (MESH:D002318), SIRD (MESH:C566531), Diabetes (MESH:D003920), DKA (MESH:D016883), respiratory disease (MESH:D012140), SIDD (MESH:D045169), non-gestational diabetes (MESH:D016640), inflammation (MESH:D007249), metabolic associated fatty liver disease (MESH:D005234), chronic kidney disease (MESH:D051436), COVID-19 (MESH:D000086382)
- **Chemicals:** DiaClue (-), Metformin (MESH:D008687), glucose (MESH:D005947)
- **Species:** Severe acute respiratory syndrome coronavirus 2 (no rank) [taxon 2697049], Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

1 figure with captions in the complete paper: https://tomesphere.com/paper/PMC13028042/full.md

## References

40 references — full list in the complete paper: https://tomesphere.com/paper/PMC13028042/full.md

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Source: https://tomesphere.com/paper/PMC13028042