Exercise Training but not Curcumin Supplementation Decreases Immune Cell Infiltration in the Pancreatic Islets of a Genetically Susceptible Model of Type 1 Diabetes

Abstract 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...

Full description

Bibliographic Details
Main Authors: Leandro Kansuke Oharomari, Camila de Moraes, Anderson Marliere Navarro
Format: Article
Language:English
Published: SpringerOpen 2017-04-01
Series:Sports Medicine - Open
Subjects:
Online Access:http://link.springer.com/article/10.1186/s40798-017-0082-3
Description
Summary:Abstract 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.
ISSN:2199-1170
2198-9761