ArticleGenes & diseases2022
Circulating exosome-like vesicles of humans with nondiabetic obesity impaired islet β-cell proliferation, which was associated with decreased Omentin-1 protein cargo.
Article in Genes & diseases, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Adipocyte-derived exosomal ANGPTL2 promotes beta cell dysfunction via the EIF2α/ATF4/CHOP stress pathway in mice.Diabetologia · 2026Article
- Editorial for the Special Issue: Feature Reviews in Adipokines.Biomedicines · 2025Article
- Elevated body fat percentage is linked to increased risk of diabetes: a longitudinal retrospective cohort study based on Chinese adults.Frontiers in nutrition · 2025Article
- The emerging role of extracellular vesicles in diabetes and complications: mechanistic insights and translational prospects.Frontiers in endocrinology · 2025Review
- The Role of Extracellular Vesicles in Metabolic Diseases.Biomedicines · 2024Review
- A Pilot Study on the Proteomics Profile of Serum Exosome-Enriched Extracellular Vesicles from Normal versus Individuals with Obesity-Related Insulin Resistance.Biomedicines · 2024Article
- Omentin: A Key Player in Glucose Homeostasis, Atheroprotection, and Anti-Inflammatory Potential for Cardiovascular Health in Obesity and Diabetes.Biomedicines · 2024Review
- An Overview of Inter-Tissue and Inter-Kingdom Communication Mediated by Extracellular Vesicles in the Regulation of Mammalian Metabolism.International journal of molecular sciences · 2023Review
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The regulation of β-cell mass in the status of nondiabetic obesity remains not well understood. We aimed to investigate the role of circulating exosome-like vesicles (ELVs) isolated from humans with simple obesity in the regulation of islet β-cell mass. Between June 2017 and July 2019, 81 subjects with simple obesity and 102 healthy volunteers with normal weight were recruited. ELVs were isolated by ultra-centrifugation. The proliferations of β-cells and islets were measured by 5-ethynl-2'-deoxyuridine (EdU). Protein components in ELVs were identified by Quantitative Proteomic Analysis and verified by Western blot and ELISA. The role of specific exosomal protein was analyzed by gain-of-function approach in ELVs released by 3T3-L1 preadipocytes. Circulating ELVs from subjects with simple obesity inhibited β-cell proliferation
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