Exercise Training but not Curcumin Supplementation Decreases Immune Cell Infiltration in the Pancreatic Islets of a Genetically Susceptible Model of Type 1 Diabetes
- PMID: 28378202
- PMCID: PMC5380567
- DOI: 10.1186/s40798-017-0082-3
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 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.
Keywords: Autoimmunity; Bioactive compound; Curcumin; Exercise training; Insulitis; Type 1 diabetes.
Figures
Similar articles
-
Suppression of insulitis in non-obese diabetic (NOD) mice by oral insulin administration is associated with selective expression of interleukin-4 and -10, transforming growth factor-beta, and prostaglandin-E.Am J Pathol. 1995 Nov;147(5):1193-9. Am J Pathol. 1995. PMID: 7485382 Free PMC article.
-
11-Keto-β-Boswellic Acid Inhibits Lymphocyte (CD3) Infiltration Into Pancreatic Islets of Young None Obese Diabetic (NOD) Mice.Horm Metab Res. 2017 Sep;49(9):693-700. doi: 10.1055/s-0043-112761. Epub 2017 Jul 31. Horm Metab Res. 2017. PMID: 28759942
-
IL-33 Prevents MLD-STZ Induction of Diabetes and Attenuate Insulitis in Prediabetic NOD Mice.Front Immunol. 2018 Nov 15;9:2646. doi: 10.3389/fimmu.2018.02646. eCollection 2018. Front Immunol. 2018. PMID: 30498495 Free PMC article.
-
Cellular and molecular roles of beta cell autoantigens, macrophages and T cells in the pathogenesis of autoimmune diabetes.Arch Pharm Res. 1999 Oct;22(5):437-47. doi: 10.1007/BF02979150. Arch Pharm Res. 1999. PMID: 10549569 Review.
-
Control of type 1 autoimmune diabetes by naturally occurring CD4+CD25+ regulatory T lymphocytes in neonatal NOD mice.Ann N Y Acad Sci. 2005 Jun;1051:72-87. doi: 10.1196/annals.1361.048. Ann N Y Acad Sci. 2005. PMID: 16126946 Review.
Cited by
-
Resistance Training Improves Beta Cell Glucose Sensing and Survival in Diabetic Models.Int J Mol Sci. 2022 Aug 21;23(16):9427. doi: 10.3390/ijms23169427. Int J Mol Sci. 2022. PMID: 36012692 Free PMC article.
-
Impacts of an Exercise Intervention on the Health of Pancreatic Beta-Cells: A Review.Int J Environ Res Public Health. 2022 Jun 13;19(12):7229. doi: 10.3390/ijerph19127229. Int J Environ Res Public Health. 2022. PMID: 35742478 Free PMC article. Review.
-
Environmental Determinants of Type 1 Diabetes: From Association to Proving Causality.Front Immunol. 2021 Oct 1;12:737964. doi: 10.3389/fimmu.2021.737964. eCollection 2021. Front Immunol. 2021. PMID: 34659229 Free PMC article. Review.
-
A Novel Promising Frontier for Human Health: The Beneficial Effects of Nutraceuticals in Cardiovascular Diseases.Int J Mol Sci. 2020 Nov 18;21(22):8706. doi: 10.3390/ijms21228706. Int J Mol Sci. 2020. PMID: 33218062 Free PMC article. Review.
References
-
- The autoimmune diseases coordinating committee (ADCC). Progress in Autoimmune Diseases Research Progress. Bethesda: National Institutes of Health; 2005. p. 1–129.
-
- Egro FM. Why is type 1 diabetes increasing? J Mol Endocrinol. 2013;51:R1–13. - PubMed
LinkOut - more resources
Full Text Sources
Other Literature Sources
