ArticleDiabetologia2025
Exercise-induced meteorin-like protein protects human pancreatic beta cells from cytokine-induced apoptosis.
Article in Diabetologia, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Exerkine-Mediated Inter-Organ Crosstalk and Translational Perspectives in Metabolic Diseases.Current obesity reports · 2026Review
- Metrnl in diabetes and its complications: divergent evidence and translational prospects.Journal of translational medicine · 2026Review
- Artificial intelligence-driven therapeutics for disease modification in type 1 diabetes: a digital public health and clinical translation framework.Frontiers in public health · 2026Review
- Association of Serum Meteorin-Like with OCTA Metrics in Type 2 Diabetic Nonproliferative Retinopathy: A Cross-Sectional Study.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Article
- Global research dynamics in the induced pluripotent stem cell and diabetes: A bibliometric analysis of the past twenty years.Regenerative therapy · 2025Article
- Identification of novel type 1 and type 2 diabetes genes by co-localization of human islet eQTL and GWAS variants with colocRedRibbon.Cell genomics · 2025Article
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Authors and funding
11 authors.
Funding
Abstract
aims/hypothesisInflammation-driven pancreatic beta cell death is a hallmark of type 1 diabetes progression. We have previously shown that serum obtained from individuals after high-intensity interval training prevents cytokine-induced human beta cell apoptosis, but the mediators of this beneficial effect remain to be characterised. In this study we evaluated the role of exercise-induced meteorin-like protein (Metrnl) in human beta cell protection.
methodsHuman EndoC-βH1 cells and induced pluripotent stem cell (iPSC)-derived islets were exposed to proinflammatory cytokines and treated with serum collected before and after high-intensity interval training, with and without Metrnl-neutralising antibodies. The effects of Metrnl on apoptosis, insulin secretion and chemokine CXCL10 gene and protein expression were assessed.
resultsPost-exercise serum had an increased concentration of Metrnl compared with pre-exercise level serum, resulting in a 46% reduction in cytokine-induced beta cell death. Additionally, direct treatment with recombinant Metrnl at concentrations of 100 ng/ml and 200 ng/ml reduced cytokine-induced cell death by 24% and 41%, respectively, in EndoC-βH1 cells, with similar results obtained in iPSC-derived islets. Metrnl treatment also preserved insulin secretion under inflammatory stress. These effects were associated with a decrease in CXCL10 mRNA expression and protein release. Blocking Metrnl with a neutralising antibody eliminated the protective effects of serum from trained individuals on EndoC-βH1 cells exposure to proinflammatory cytokines. CONCLUSIONS/
interpretationOur findings reveal that the exerkine Metrnl is a key mediator of the beneficial effects of exercise on pancreatic beta cells, suggesting that Metrnl is a potential therapeutic target for preserving human beta cell function and survival in type 1 diabetes.
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