|Publication status||Published - 1 Jul 2012|
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TY - ADVS
T1 - Metabolomics Approach for Analyzing the Effects of Exercise in Subjects with Type 1 Diabetes Mellitus
AU - Brugnara, Laura
AU - Vinaixa, Maria
AU - Murillo, Serafin
AU - Samino, Sara
AU - Rodriguez, Miguel Angel
AU - Beltran, Antoni
AU - Lerin, Carles
AU - Davison, Gareth
AU - Correig, Xavier
AU - Novials, Anna
N1 - Reference text: 1. DCCT/EDIC - Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications (DCCT/EDIC) Study Research Group (2005) Intensive diabetes treatment and cardiovascular disease in patients with type 1 diabetes. N Engl J Med 353: 2643–2653. 2. DPP - Diabetes Prevention Program Research Group (2002) Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin.N Engl J Med 346: 393–403. 3. Pan XR, Li GW, Hu YH, Wang JX, Yang WY, et al. (1997) Effects of diet and exercise in preventing NIDDM in people with impaired glucose tolerance. The Da Qing IGT and Diabetes Study. Diabetes Care 20: 537–544. 4. Tuomilehto J, Lindstro¨m J, Eriksson J, Valle TT, Ha¨ma¨ la¨ inen H, et al. (2001) Prevention of type 2 diabetes by changes in lifestyle among subjects with impaired glucose tolerance. N Engl J Med 344: 1343–1350. 5. Thompson PD, Buchner D, Pin˜a IL, Balady GJ, Williams MA, et al. 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(2010) Insulin resistance in adolescents with type 1 diabetes and its relationship to cardiovascular function. J Clin Endocrinol Metab, 95: 513–521. 39. Perseghin G, Lattuada G, Danna M, Sereni LP, Maffi P, et al. (2003) Insulin resistance, intramyocellular lipid content, and plasma adiponectin in patients with type 1 diabetes. Am J Physiol Endocrinol Metab 285: E1174–1181. 40. Levin K, Daa Schroeder H, Alford FP, Beck-Nielsen H (2001) Morphometric documentation of abnormal intramyocellular fat storage and reduced glycogen in obese patients with Type II diabetes. Diabetologia, 44: 824–833. 41. Kelley DE, Mandarino LJ (2000) Fuel selection in human skeletal muscle in insulin resistance: a reexamination. Diabetes 49: 677–683. 42. Galgani JE, Moro C, Ravussin E (2008) Metabolic flexibility and insulin resistance. Am J Physiol Endocrinol Metab 295: E1009–1017. 43. Mogensen M, Sahlin K, Fernstro¨m M, Glintborg D, Vind BF, et al. (2007) Mitochondrial respiration is decreased in skeletal muscle of patients with type 2 diabetes. Diabetes 56: 1592–1599. 44. Befroy DE, Petersen KF, Dufour S, Mason GF, de Graaf RA, et al. (2007) Impaired mitochondrial substrate oxidation in muscle of insulin-resistant offspring of type 2 diabetic patients. Diabetes 56: 1376–1381. 45. Item F, Heinzer-Schweize S, Wyss M, Fontana P, Lehmann R, et al. (2011) Mitochondrial capacity is affected by glycemic status in young untrained women with type 1 diabetes but is not impaired relative to healthy untrained women Am J Physiol Regul Integr Comp Physiol 301: R60–R66. 46. Morino K, Petersen KF, Shulman GI (2006) Molecular mechanisms of insulin resistance in humans and their potential links with mitochondrial dysfunction. Diabetes 55 (Suppl 2): S9–S15. 47. Farhy LS, Chan A, Breton MD, Anderson SM, Kovatchev BP, et al. (2012) Association of Basal hyperglucagonemia with impaired glucagon counterregulation in type 1 diabetes. Front Physiol.3:40, doi: 10.3389/fphys.2012.00040. 48. Divertie GD, Jensen MD, Cryer PE, Miles JM (1997) Lipolytic responsiveness to epinephrine in nondiabetic and diabetic humans. Am J Physiol, 272: E1130–1135. 49. Komatsu WR, Gabbay MA, Castro ML, Saraiva GL, Chacra AR, et al. (2005) Aerobic exercise capacity in normal adolescents and those with type 1 diabetes mellitus. Pediatr Diabetes 6: 145–149. 50. Gusso S, Hofman P, Lalande S, Cutfield W, Robinson E, et al. (2008) Impaired stroke volume and aerobic capacity in female adolescents with type 1 and type 2 diabetes mellitus. Diabetologia 51: 1317–1320. 51. Vervoort G, Wetzels JF, Lutterman JA, van Doorn LG, Berden JH, et al. (1999) Elevated skeletal muscle blood flow in noncomplicated type 1 diabetes mellitus: role of nitric oxide and sympathetic tone. Hypertension 34: 1080–1085.
PY - 2012/7/1
Y1 - 2012/7/1
N2 - The beneficial effects of exercise in patients with type 1 diabetes (T1D) are not fully proven, given that it may occasionally induce acute metabolic disturbances. Indeed, the metabolic disturbances associated with sustained exercise may lead to worsening control unless great care is taken to adjust carbohydrate intake and insulin dosage. In this work, pre- and postexercise metabolites were analyzed using a 1H-NMR and GC-MS untargeted metabolomics approach assayed in serum. We studied ten men with T1D and eleven controls matched for age, body mass index, body fat composition, and cardiorespiratory capacity, participated in the study. The participants performed 30 minutes of exercise on a cycleergometer at 80% VO2max. In response to exercise, both groups had increased concentrations of gluconeogenic precursors (alanine and lactate) and tricarboxylic acid cycle intermediates (citrate, malate, fumarate and succinate). The T1D group, however, showed attenuation in the response of these metabolites to exercise. Conversely to T1D, the control group also presented increases in a-ketoglutarate, alpha-ketoisocaproic acid, and lipolysis products (glycerol and oleic and linoleic acids), as well as a reduction in branched chain amino acids (valine and leucine) determinations. The T1D patients presented a blunted metabolic response to acute exercise as compared to controls. This attenuated response may interfere in the healthy performance or fitness of T1D patients, something that further studies should elucidate.
AB - The beneficial effects of exercise in patients with type 1 diabetes (T1D) are not fully proven, given that it may occasionally induce acute metabolic disturbances. Indeed, the metabolic disturbances associated with sustained exercise may lead to worsening control unless great care is taken to adjust carbohydrate intake and insulin dosage. In this work, pre- and postexercise metabolites were analyzed using a 1H-NMR and GC-MS untargeted metabolomics approach assayed in serum. We studied ten men with T1D and eleven controls matched for age, body mass index, body fat composition, and cardiorespiratory capacity, participated in the study. The participants performed 30 minutes of exercise on a cycleergometer at 80% VO2max. In response to exercise, both groups had increased concentrations of gluconeogenic precursors (alanine and lactate) and tricarboxylic acid cycle intermediates (citrate, malate, fumarate and succinate). The T1D group, however, showed attenuation in the response of these metabolites to exercise. Conversely to T1D, the control group also presented increases in a-ketoglutarate, alpha-ketoisocaproic acid, and lipolysis products (glycerol and oleic and linoleic acids), as well as a reduction in branched chain amino acids (valine and leucine) determinations. The T1D patients presented a blunted metabolic response to acute exercise as compared to controls. This attenuated response may interfere in the healthy performance or fitness of T1D patients, something that further studies should elucidate.
U2 - 10.1371/journal.pone.0040600
DO - 10.1371/journal.pone.0040600
M3 - Web publication/site