Abstract
BackgroundThe 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.MethodsTo 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).ResultsModerate 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.ConclusionsThese data provide evidence that exercise training can mitigate T1D development in genetically susceptible mice.
Highlights
The main mechanism involved in the pathogenesis of autoimmunity is an uncontrolled inflammatory response against self-antigens
Insulin levels tended to be lower in curcumin supplementation (CUR) and T, but the difference only reached a statistical level of significance in the trained + curcumin supplementation (TC) group
homeostatic model assessment of insulin resistance (HOMA-IR) was not modified by curcumin or exercise training (Table 1)
Summary
The main mechanism involved in the pathogenesis of autoimmunity is an uncontrolled inflammatory response against self-antigens. 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. Intense inflammatory response is a main feature of autoimmune diseases. Type 1 diabetes (T1D), for instance, occurs due to a chronic inflammatory response with enough severity to destroy most of the pancreatic β cells [1]. Physical inactivity and processed food intake during childhood appear to be linked to the development of chronic [8,9,10] and inflammatory disease [11] in early stages of life. The Overload Hypothesis suggests an association between a modern lifestyle and beta
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