Aim of the work: Diabetes is characterized by progressive loss of functional pancreatic beta cells. None of the therapeutic agents used to treat diabetes arrest this process and preventing beta cell loss remains a major unmet need. We have previously shown that serum from 8 young healthy males who exercised for 8 weeks protects human islets and human insulin-producing EndoC-βH1 cells from apoptosis induced by pro-inflammatory cytokines or the endoplasmic reticulum (ER) stressor thapsigargin. Whether this protective effect is influenced by sex, age, training modality, ancestry and diabetes is unknown.
Methods: We enrolled 82 individuals, male or female, nondiabetic or diabetic, from different origins, in different supervised training protocols for 8-12 weeks (including training at home during the COVID-19 pandemic). EndoC-βH1 cells were treated with exercised serum to ascertain cytoprotection from ER stress.
Results: The exercise interventions were effective and improved VO2 peak values in both younger and older, non-obese and obese, non-diabetic and diabetic participants. Serum obtained after training conferred significant beta cell protection from severe ER stress-induced apoptosis. Cytoprotection was not affected by the type of exercise training or participant age, sex, BMI or ancestry, and persisted for up to 2 months after the end of the training program. Serum from exercised patients with type 1 or type 2 diabetes was similarly protective.
Conclusions: These data uncover the unexpected potential to preserve beta cell health by exercise training, opening a new avenue to prevent or slow diabetes progression through humoral muscle-beta cell crosstalk.