Subscribe to RSS
DOI: 10.1055/s-0034-1372581
Importance of Exercise in the Control of Metabolic and Inflammatory Parameters at the Moment of Onset in Type 1 Diabetic Subjects
Publication History
received 16 January 2014
first decision 04 March 2014
accepted 19 March 2014
Publication Date:
05 May 2014 (online)
Abstract
The onset of type 1 diabetes coincides with the final phase of β-cell destruction. In some cases, this period is characterized by the presence of a functional reserve of β-cells, favouring an adequate metabolic control (honeymoon phase). Therefore, the extension of this situation could have evident benefits in subsequent diabetes management. We aimed to study the influence of regular physical activity before and after the onset of the disease. We did an observational study of 2 groups of type 1 diabetic patients from onset to a 2-year period. One group (n=8) exercised regularly (5 or more hours/week) before onset and continued doing so with the same regularity. The second group (n=11) either did not perform physical activity or did so sporadically. Circulating glycated haemoglobin (HbA1c), C-peptide, protein carbonyls and basal cytokine levels were determined at the beginning and at the end of the 1st and 2nd year. The more active group debuted with and maintained significantly lower HbA1c levels and insulin requirements compared to the more sedentary group. C-peptide levels were only significantly higher in the active group at the moment of onset compared to the sedentary group. In addition, determination of basal circulating cytokines revealed a large variability between individuals but no significant differences when comparing the groups. Altogether, the obtained results seem to indicate that physical activity allows a better control at the moment of onset regarding glycaemic control, residual endocrine pancreatic mass and subsequent insulin requirements.
-
References
- 1 Boitard C. Pancreatic islet autoimmunity. Presse Med 2012; 41: e636-e650
- 2 Notkins AL. Immunologic and genetic factors in type 1 diabetes. J Biol Chem 2002; 277: 43545-43548
- 3 Rabinovitch A, Suarez-Pinzon WL. Role of cytokines in the pathogenesis of autoimmune diabetes mellitus. Rev Endocr Metab Disord 2003; 4: 291-299
- 4 Nathan DM, Zinman B, Cleary PA et al. DCCT/EDIC Groups. Modern-day clinical course of type 1 diabetes mellitus after 30 years’ duration: the diabetes control and complications trial/epidemiology of diabetes interventions and complications and Pittsburgh epidemiology of diabetes complications experience (1983–2005). Arch Intern Med 2009; 169: 1307-1316
- 5 Gupta S. Immunotherapies in diabetes mellitus type 1. Med Clin North Am 2012; 96: 621-634
- 6 Ludvigsson J. Novel therapies in the management of type I diabetes mellitus. Panminerva Med 2012; 54: 257-270
- 7 Gallagher MP, Goland RS, Greenbaum CJ. Making progress: preserving beta cells in type 1 diabetes. Ann N Y Acad Sci 2011; 1243: 119-134
- 8 Sethi G, Sung B, Kunnumakkara AB et al. for Treatment of Cancer and Autoimmunity. Adv Exp Med Biol 2009; 647: 37-51
- 9 Nielsen PJ, Hafdahl AR, Conn VS et al. Meta-analysis of the effect of exercise interventions on fitness outcomes among adults with type 1 and type 2 diabetes. Diabetes Res Clin Pract 2006; 74: 111-120
- 10 Conn VS, Hafdahl AR, Lemaster JW et al. Meta-analysis of health behavior change interventions in type 1 diabetes. Am J Health Behav 2008; 32: 315-329
- 11 Jakicic JM, Clark K, Coleman E et al. American College of Sports Medicine position stand. Appropriate intervention strategies for weight loss and prevention of weight regain for adults. Med Sci Sports Exerc 2001; 33: 2145-2156
- 12 Levine RL, Williams JA, Stadtman ER et al. Carbonyl assays for determination of oxidatively modified proteins. Methods Enzymol 1994; 233: 346-357
- 13 International Expert Committee report on the role of the A1C assay in the diagnosis of diabetes . Diabetes Care 2009; 32: 1327-1334
- 14 American Diabetes Association . Diagnosis and classification of diabetes mellitus. Diabetes Care 2010; 33 (Suppl. 01) S62-S69
- 15 Ali MA, Dayan CM. The importance of residual endogenous beta-cell preservation in type 1 diabetes. Br J Diab Vasc Dis 2009; 9: 248-253
- 16 Mortensen HB, Hougaard P, Swift P et al. Hvidoere Study Group on Childhood Diabetes. New definition for the partial remission period in children and adolescents with type 1 diabetes. Diabetes Care 2009; 32: 1384-1390
- 17 Robertson RP. Chronic oxidative stress as a central mechanism for glucose toxicity in pancreatic islet beta cells in diabetes. J Biol Chem 2004; 279: 42351-42354
- 18 van Belle TL, Coppieters KT, von Herrath MG. Type 1 diabetes: etiology, immunology, and therapeutic strategies. Physiol Rev 2011; 91: 79-118
- 19 Ludvigsson J. Therapy with GAD in diabetes. Diabetes Metab Res Rev 2009; 25: 307-315
- 20 Baumann B, Salem HH, Boehm BO. Anti-inflammatory therapy in type 1 diabetes. Curr Diab Rep 2012; 12: 499-509
- 21 Fredheim S, Johansen J, Johansen A et al. Danish Society for Diabetes in Childhood and Adolescence. Diabetic ketoacidosis at the onset of type 1 diabetes is associated with future HbA1c levels. Diabetologia 2013; 56: 995-1003
- 22 Niess AM, Simon P. Response and adaptation of skeletal muscle to exercise – the role of reactive oxygen species. Front Biosci 2007; 12: 4826-4838
- 23 Hirose L, Nosaka K, Newton M et al. Changes in inflammatory mediators following eccentric exercise of the elbow flexors. Exerc Immunol Rev 2004; 10: 75-90
- 24 Malm C. Exercise immunology: the current state of man and mouse. Sports Med 2004; 34: 555-566
- 25 Toft AD, Jensen LB, Bruunsgaard H et al. Cytokine response to eccentric exercise in young and elderly humans. Am J Physiol Cell Physiol 2002; 283: C289-C295
- 26 Singh B, Nikoopour E, Huszarik K et al. Immunomodulation and regeneration of islet beta cells by cytokines and autoimmune type 1 diabetes. J Interf Cytok Res 2011; 31: 711-719
- 27 Yamanouchi J, Rainbow D, Serra P et al. Interleukin-2 gene variation impairs regulatory T cell function and causes autoimmunity. Nat Genet 2007; 39: 329-337
- 28 Sgouroudis E, Albanese A, Piccirillo CA. Impact of protective IL-2 allelic variants on CD4+Foxp3+regulatory T cell function in situ and resistance to autoimmune diabetes in NOD mice. J Immunol 2008; 181: 6283-6292
- 29 Grinberg-Bleyer Y, Baeyens A, You S et al. IL-2 reverses established type 1 diabetes in NOD mice by a local effect on pancreatic regulatory T cells. J Exp Med 2010; 207: 1871-1878
- 30 Tang Q, Adams JY, Penaranda C et al. Central role of defective interleukin-2 production in the triggering of islet autoimmune destruction. Immunity 2008; 28: 687-697
- 31 Rapoport MJ, Jaramillo A, Zipris D et al. Interleukin 4 reverses T cell proliferative unresponsiveness and prevents the onset of diabetes in nonobese diabetic mice. J Exp Med 1993; 178: 87-99
- 32 Goudy KS, Burkhardt BR, Wasserfall C et al. Systemic overexpression of IL-10 induces CD4+CD25+cell populations in vivo and ameliorates type 1 diabetes in nonobese diabetic mice in a dose-dependent fashion. J Immunol 2003; 171: 2270-2278
- 33 Hillhouse EE, Beauchamp C, Chabot-Roy G et al. Interleukin-10 limits the expansion of immunoregulatory CD4-CD8- T cells in autoimmune-prone non-obese diabetic mice. Immunol Cell Biol 2010; 88: 771-780
- 34 Xiong X, Wang X, Li B et al. Pancreatic islet-specific overexpression of Reg3β protein induced the expression of pro-islet genes and protected the mice against streptozotocin-induced diabetes mellitus. Am J Physiol Endocrinol Metab 2011; 300: E669-E680
- 35 Vicente-Salar N, Santana A, Reig J et al. Differentiation of embryonic stem cells using pancreatic bud-conditioned medium gives rise to neuroectoderm-derived insulin-secreting cells. Cell Reprogram 2011; 13: 77-84
- 36 Shioya M, Andoh A, Kakinoki S et al. Interleukin 22 receptor 1 expression in pancreas islets. Pancreas 2008; 36: 197-199
- 37 Rosa JS, Oliver SR, Mitsuhashi M et al. Altered kinetics of interleukin-6 and other inflammatory mediators during exercise in children with type 1 diabetes. J Investig Med 2008; 56: 701-713
- 38 Luo C, Li B, Yin HP et al. Transcriptional activation of Reg2 and Reg3β genes by glucocorticoids and interleukin-6 in pancreatic acinar and islet cells. Mol Cell Endocrinol 2012; 365: 187-196