ORIGINAL RESEARCH article
Front. Cell. Infect. Microbiol.
Sec. Intestinal Microbiome
Volume 15 - 2025 | doi: 10.3389/fcimb.2025.1606652
This article is part of the Research TopicGut Microbiota and Age-Related Disorders: From Mechanisms to TherapiesView all 8 articles
Exercise improves endothelial progenitor cell's function in mice with Type 2 diabetes via gut microbiota modulation
Provisionally accepted
- 1Department of Endocrinology, First Affiliated Hospital of Guangxi Medical University, Nanning, China
- 2First Affiliated Hospital, Guangxi Medical University, Nanning, Guangxi Zhuang Region, China
- 3Baise City People's Hospital, Baise, Guangxi Zhuang Region, China
- 4Affiliated Tumor Hospital of Guangxi Medical University, Nanning, Guangxi Zhuang Region, China
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This study explored the mechanism by which exercise improves endothelial progenitor cells (EPCs) function in type 2 diabetic (db/db) mice, focusing on gut microbiota mediation. Exercise altered microbial composition (e.g., increased Prevotellaceae and Ligilactobacillus), while fecal microbiota transplantation(FMT) enriched Akkermansia. Notably, FMT elevated plasma Glucagon-like peptide-1 (GLP-1) levels by 0.92 pmmol/L (P < 0.001) compared to controls, surpassing the modest, non-significant effects of exercise alone. Critically, FMT enhanced EPC's proliferation (P < 0.007 vs. controls) and migration (P < 0.05), mirroring exercise-induced improvements. While exercise reduced body weight (e.g., 10.58 g in aerobic training (AT), P < 0.001) and blood glucose, FMT amplified these metabolic benefits, lowering glucose by 9.22 mmol/L (P < 0.001). Our findings suggest that exercise improves EPC's function in diabetic mice via gut microbiota modulation, with FMT synergistically enhancing GLP-1 secretion. The identified microbiota (Prevotellaceae, Ligilactobacillus, Akkermansia) may serve as therapeutic targets for T2DM(T2DM) and its cardiovascular complications.
Keywords: Exercise, diabetes, fecal microbiota transplantation, endothelial progenitor cells, GLP-1
Received: 06 Apr 2025; Accepted: 04 Aug 2025.
Copyright: © 2025 Dai, Chen, Zhang, Yang, Huang and Tang. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Xia Dai, Department of Endocrinology, First Affiliated Hospital of Guangxi Medical University, Nanning, China
LiAn Tang, First Affiliated Hospital, Guangxi Medical University, Nanning, 530021, Guangxi Zhuang Region, China
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