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Endocrine Abstracts (2022) 88 001 | DOI: 10.1530/endoabs.88.001

BES2022 BES 2022 Abstracts (23 abstracts)

Exercise as a non-pharmacological intervention to protect pancreatic beta cells in patients with type 1 and type 2 diabetes

Coomans de Brachène Alexandra 1 , Scoubeau Corentin 2 , Musuaya Anyïshai E 1 , Castela Angela 1 , Carpentier Julie 2 , Faoro Vitalie 3 , Klass Malgorzata 2,4 , Cnop Miriam 1,5 & Eizirik Decio L 1

1ULB Center for Diabetes Research, Medical Faculty, Université Libre de Bruxelles, Brussels, Belgium; 2Laboratory for Biometry and Exercise Nutrition, Université Libre de Bruxelles, Brussels, Belgium; 3Cardiopulmonary Exercise Laboratory, Université Libre de Bruxelles, Brussels, Belgium; 4Laboratory of Applied Biology and Research Unit in Applied Neurophysiology, Université Libre de Bruxelles, Brussels, Belgium; 5Division of Endocrinology, Erasmus Hospital, Université Libre de Bruxelles, Brussels, Belgium

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.

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