Plasma circulating miR-23~27~24 clusters correlate with the immunometabolic derangement and predict C-peptide loss in children with type 1 diabetes
Open accessAbstract
Aims/hypothesis We aimed to analyse the association between plasma circulating microRNAs (miRNAs) and the immunometabolic profile in children with type 1 diabetes and to identify a composite signature of miRNAs/immunometabolic factors able to predict type 1 diabetes progression. Methods Plasma samples were obtained from children at diagnosis of type 1 diabetes (n = 88) and at 12 (n = 32) and 24 (n = 30) months after disease onset and from healthy control children with similar sex and age distribution (n = 47). We quantified 60 robustly expressed plasma circulating miRNAs by quantitative RT-PCR and nine plasma immunometabolic factors with a recognised role at the interface of metabolic and immune alterations in type 1 diabetes. Based on fasting C-peptide loss over time, children with type 1 diabetes were stratified into the following groups: those who had lost >90% of C-peptide compared with diagnosis level; those who had lost <10% of C-peptide; those showing an intermediate C-peptide loss. To evaluate the modulation of plasma circulating miRNAs during the course of type 1 diabetes, logistic regression models were implemented and the correlation between miRNAs and immunometabolic factors was also assessed. Results were then validated in an independent cohort of children with recent-onset type 1 diabetes (n = 18). The prognostic value of the identified plasma signature was tested by a neural network-based model. Results Plasma circulating miR-23~27~24 clusters (miR-23a-3p, miR-23b-3p, miR-24-3p, miR-27a-3p and miR-27b-3p) were upmodulated upon type 1 diabetes progression, showed positive correlation with osteoprotegerin (OPG) and were negatively correlated with soluble CD40 ligand, resistin, myeloperoxidase and soluble TNF receptor in children with type 1 diabetes but not in healthy children. The combination of plasma circulating miR-23a-3p, miR-23b-3p, miR-24-3p, miR-27b-3p and OPG, quantified at disease onset, showed a significant capability to predict the decline in insulin secretion 12 months after disease diagnosis in two independent cohorts of children with type 1 diabetes. Conclusions/interpretations We have pinpointed a novel miR-23a-3p/miR-23b-3p/miR-24-3p/miR-27b-3p/OPG plasma signature that may be developed into a novel blood-based method to better stratify patients with type 1 diabetes and predict C-peptide loss.
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miR-23-3p is implicated in the occurrence and development of diabetes as a regulatory hub.
“Additionally, miR-23–3p is implicated in the occurrence and development of diabetes as a regulatory hub [14,15].”
From Recent advances of miR-23 in human diseases and growth development (2025) · cites this paper as [14]
The Results report that miR-23a-3p and miR-23b-3p increase during progression of type 1 diabetes in children, supporting an association with disease progression. The Discussion says the clusters may cooperatively affect systemic pathways, but explicitly leaves their role in causing or driving disease for future study. It does not establish miR-23-3p as a regulatory hub in the occurrence and development of diabetes generally. Page numbers are unavailable in our copy. (LLM, conf=0.87)
Experimental — accuracy not yet measuredUp-regulated expression of miR-23 has been observed in the plasma of patients with type 1 diabetes and type 2 diabetes mellitus.
“up-regulated expression of miR-23 has been witnessed in the plasma of patients with type 1 diabetes (T1DM) and type 2 diabetes mellitus (T2DM).”
From Recent advances of miR-23 in human diseases and growth development (2025) · cites this paper as [14]
The ‘Plasma circulating miRNA dysregulation during the course of type 1 diabetes’ section reports increased plasma miR-23a-3p and miR-23b-3p as type 1 diabetes progressed in children. It also says these miRNAs were not significantly different from healthy controls; the paper does not report increased plasma miR-23 in patients with type 2 diabetes. Page numbers were not available in our copy. (LLM, conf=0.88)
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- Authors
- Garavelli, S., Bruzzaniti, S., Tagliabue, E., Di Silvestre, D., Prattichizzo, F., Mozzillo, E., Fattorusso, V., La Sala, L., Ceriello, A., Puca, A. A., Mauri, P., Strollo, R., Marigliano, M., Maffeis, C., Petrelli, A., Bosi, E., Franzese, A., Galgani, M., Matarese, G., & de Candia, P.
- Affiliations
- MultiMedica (IT)
- Institute for Experimental Endocrinology and Oncology (IT)
- Federico II University Hospital (IT)
- University of Salerno (IT)
- Institute of Biomedical Technologies (IT)
- Università Campus Bio-Medico (IT)
- University of Verona (IT)
- IRCCS Ospedale San Raffaele (IT)
- Vita-Salute San Raffaele University (IT)
- Corresponding author
- Galgani, Mario
- Matarese, Giuseppe
- ORCID
- Garavelli, Silvia
- Bruzzaniti, Sara
- Tagliabue, Elena
- Prattichizzo, Francesco
- Mozzillo, Enza
- Fattorusso, Valentina
- Ceriello, Antonio
- Puca, Annibale A.
- Mauri, Pierluigi
- Strollo, Rocky
- Marigliano, Marco
- Maffeis, Claudio
- Petrelli, Alessandra
- Bosi, Emanuele
- Franzese, Adriana
- Galgani, Mario
- Matarese, Giuseppe
- de Candia, Paola
- Venue
- Diabetologia
- Published
- 2020-07-29
- Volume
- 63
- Issue
- 12
- Pages
- 2699-2712
- ISSN
- 0012-186X (ISSN-L)
- 1432-0428
- OpenAlex
- W3046083407
- Cited by
- 37
- References
- 62
- Citations by year
- 2026: 2 · 2025: 5 · 2024: 7 · 2023: 8 · 2022: 4 · 2021: 8 · 2020: 3
- FWCI
- 3.36
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Diabetologia (publishedVersion)
- PubMed (publishedVersion)
- Archivio Istituzionale della Ricerca - Università Vita-Salute San Raffaele (submittedVersion)
- Funders
- Juvenile Diabetes Research Foundation (2-SRA-2018-479-S-B)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Diabetes and associated disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Keywords
- type 1 diabetes, children, circulating microRNAs, miR-23a-3p, miR-23b-3p, miR-24-3p, miR-27b-3p, osteoprotegerin, soluble CD40 ligand, resistin, myeloperoxidase, soluble TNF receptors, disease progression prediction
- MeSH terms
- C-Peptide, Diabetes Mellitus, Type 1, Humans, MicroRNAs, Diabetes Complications, Osteoprotegerin
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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