“Splashes of Health: How Swimming Boosts Blood Vessel Growth and Fights Type 2 Diabetes in Rats”

The current research sought to examine the influence of swimming training on the angiogenesis of endothelial progenitor cells (EPCs) in rats with type 2 diabetes mellitus (T2DM) by enhancing the expression of insulin‑like growth factor 1 (IGF1) and to uncover its possible mechanisms. Male Sprague‑Dawley rats were categorized into several groups: Control, Model, Model train, Model train + short interfering (si)‑NC, and Model train + si‑IGF1. Serum glucose concentrations were assessed using the oral glucose tolerance test. EPCs were extracted from the bone marrow cavity and identified via morphological observations and immunofluorescence staining techniques. The level of IGF‑1 mRNA in rat serum and EPCs was evaluated using reverse transcription‑quantitative PCR. Fasting insulin concentrations in serum were measured by ELISA. Cell Counting Kit‑8, scratch assay, and tube formation assay methodologies were utilized to assess EPCs’ viability, migration, and tube formation capability, while western blotting was applied to determine the expression levels of IGF1, phosphoinositide 3‑kinase (PI3K), phosphorylated‑PI3K, protein kinase B (AKT), and phosphorylated‑AKT. The findings of this study indicated that swimming training considerably reduced glucose levels and homeostatic model assessment scores for insulin resistance, while increasing fasting insulin levels and IGF1 mRNA expression. Microscopic assessment and immunofluorescence identification confirmed successful isolation of EPCs. Additionally, swimming training significantly raised IGF1 levels and enhanced cell viability, migration, and tube formation in rat EPCs. Furthermore, IGF1 knockdown experiments suggested that swimming training may regulate by enhancing IGF1 expression to activate the PI3K/AKT signaling pathway. In summary, swimming training enhanced EPC angiogenesis in T2DM rats, and its potential mechanism could be associated with the upregulation of IGF1 expression and the activation of the PI3K/AKT pathway.