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Exercise improves endothelial progenitor cell's function in mice with Type 2 diabetes via gut microbiota modulation
Xia Dai1, Haiyan Chen2, Milei Zhang3
1Department of Endocrinology, The First Affiliated Hospital of Guangxi Medical University, Nanning, China.
Frontiers in Cellular and Infection Microbiology
|September 15, 2025
Summary
Exercise improves endothelial progenitor cell (EPC) function in diabetic mice by altering gut microbiota. Fecal microbiota transplantation (FMT) enhances this effect, boosting GLP-1 and improving metabolic health.
Area of Science:
- Microbiology
- Endocrinology
- Exercise Physiology
Background:
- Exercise enhances endothelial progenitor cell (EPC) migration and tube formation.
- The precise mechanisms by which exercise improves EPC function remain unclear, particularly in the context of type 2 diabetes (T2DM).
Purpose of the Study:
- To investigate the role of gut microbiota in mediating exercise-induced improvements in EPC function in type 2 diabetic mice.
- To assess the impact of fecal microbiota transplantation (FMT) on GLP-1 secretion, metabolic parameters, and EPC function.
Main Methods:
- Conducted 8-week exercise interventions (aerobic, resistance, combined) in type 2 diabetic mice.
- Performed FMT from exercise-conditioned mice to recipient mice.
- Evaluated changes in glucose, body weight, GLP-1 levels, gut microbiota composition, and EPC proliferation/migration.
Main Results:
- Exercise altered gut microbial composition, enriching beneficial bacteria like Prevotellaceae and Ligilactobacillus.
- FMT significantly increased plasma GLP-1 levels and enhanced EPC proliferation and migration.
- FMT amplified exercise-induced metabolic benefits, including significant reductions in body weight and blood glucose.
Conclusions:
- Exercise improves EPC function in diabetic mice primarily through gut microbiota modulation.
- FMT synergistically enhances GLP-1 secretion and EPC function, offering a potential therapeutic strategy.
- Specific gut microbes (Prevotellaceae, Ligilactobacillus, Akkermansia) are identified as potential therapeutic targets for T2DM and its cardiovascular complications.
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