Cargando…
Exercise Training but not Curcumin Supplementation Decreases Immune Cell Infiltration in the Pancreatic Islets of a Genetically Susceptible Model of Type 1 Diabetes
BACKGROUND: The main mechanism involved in the pathogenesis of autoimmunity is an uncontrolled inflammatory response against self-antigens. Therefore, anti-inflammatory factors, such as the intake of bioactive compounds and a physically active lifestyle, may decrease or cease the development of auto...
Autores principales: | , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Springer International Publishing
2017
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5380567/ https://www.ncbi.nlm.nih.gov/pubmed/28378202 http://dx.doi.org/10.1186/s40798-017-0082-3 |
Sumario: | BACKGROUND: The main mechanism involved in the pathogenesis of autoimmunity is an uncontrolled inflammatory response against self-antigens. Therefore, anti-inflammatory factors, such as the intake of bioactive compounds and a physically active lifestyle, may decrease or cease the development of autoimmune diseases. Type 1 diabetes (T1D) is an autoimmune disease characterized by pancreatic β cell destruction. The non-obese diabetic (NOD) mouse is a model of spontaneous T1D and is the model most similar to human disease. METHODS: To determine the effects of exercise training and curcumin supplementation on T1D progression, 48 NOD mice, 5 weeks old, were randomly divided into four groups: control, curcumin supplementation, trained, and trained plus curcumin. Every 2 weeks, blood glucose was measured using a glucometer. At the end of 20 weeks, a histopathological procedure was used to assess immune cells infiltration into pancreatic β cells (insulitis). RESULTS: Moderate intensity exercise training has the potential to protect pancreatic β cells against an immune response in vivo. However, curcumin supplementation failed to attenuate insulitis in NOD mice. CONCLUSIONS: These data provide evidence that exercise training can mitigate T1D development in genetically susceptible mice. |
---|