679-P: Endothelial and Hematopoietic Progenitor Cells Are Reduced at Rest and Have an Attenuated Mobilization Response to Exercise in People with Type 1 Diabetes

Aims: Endothelial and Hematopoietic Progenitor Cells (EPCs and HPCs) promote vascular health through secreting proangiogenic factors and replacing damaged cells. Exercise has been shown to be a mobiliser of these rare cells in healthy individuals, however, the response in chronic diseases such as type 1 diabetes (T1D) is unclear. We compared EPC and HPC counts at rest and after acute exercise in people with and without T1D. Methods: Thirty T1D participants (38±12 years, HbA1c 58.5±9.3 mmol/mol-1, diabetes duration 20±13 years) and 30 age, sex, BMI and fitness matched non diabetes controls were recruited. After a maximal exercise test, participants attended a second visit to complete 45mins of walking at 60%VO2peak. Blood samples were taken at rest, immediately and 1 hour post exercise. Circulating levels of two HPCs and five EPC phenotypes were enumerated by flow cytometry. Data (mean±SD) were analysed by mixed model ANOVA and t-test with significance accepted at p≤0.05. Results: The T1D group had significantly lower rest count of HPCs and EPCs, ranging from 21 to 41% lower across all samples compared to the control. Exercise mobilized all cell phenotypes in both groups, with significant increases from rest to post exercise, while HPCs and CD34+CD31+ EPCs remained elevated 1hr post exercise. However, the change (Δ) in HPCs and EPCs from rest to post exercise was greater in the control versus T1D group, with higher CD34+CD45dim HPCs (p=0.03, Δ 48±65 vs. 24±33 cells/ml), as well as CD34+CD31+ (p=0.04, Δ 23±19 vs. 15±25 cells/ml) and CD34+VEGFR2+ EPCs (p=0.02, Δ 24 ±24 vs. 15±31 cells/ml). Conclusion: People with T1D have reduced numbers of HPCs and EPCs at rest and also display a blunted exercise induced increase in these rare blood vessel protecting cells. Further research is needed to understand the clinical significance of an attenuated exercise mobilization of these EPCs and HPCs phenotypes in predicting future cardiovascular complications in T1D. Disclosure G.S. Taylor: None. K. Smith: None. J. Scragg: None. A. Bashir: None. A. Flatt: None. E.J. Stevenson: None. J.A. Shaw: Advisory Panel; Self; Medtronic. Speaker’s Bureau; Self; Novo Nordisk A/S. M.D. Ross: None. D.J. West: None. Funding Diabetes Research & Wellness Foundation (to D.J.W.)