Changes in Muscle Biomarkers Following Swimming Exercise in Streptozotocin-induced Rats
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[PURPOSE] The purpose of this study was to assess the effect of swimming exercise in diabetic atrophy by monitoring changes in biomarkers associated with musculoskeletal growth and abnormalities. [METHODS] Ninety-two male Sprague-Dawley rats were randomly divided into four groups: control plus exercise group (CO+Ex), control and no exercise group (CO+No Ex), diabetes plus exercise group (DM+Ex) and diabetes and no exercise group (DM+No Ex). Swimming exercise was implemented for 60 min/day, 5 day/week for a total of eight weeks. Muscle strength and atrophy biomarkers as well as muscle morphology were compared at the first, second, fourth and eighth week of experimentation. [RESULTS] ACE levels were significantly higher in the DM groups (p<.05), however swimming exercise did not significantly affect ACE levels. Irisin levels were significantly higher in the DM and DM+Ex groups compared to the CON, in week one (p<.05), and greater in the DM+Ex group at week two compared to CON+Ex (p<.05), but swimming did not significantly affect irisin levels over the eight-week period in DM rats. In terms of muscle damage, Myl3 expression was unchanged in the CON groups, but significantly higher in the DM+Ex group compared to the CON+Ex group (p<.05). AST was found to be in higher levels in the DM+No Ex group, compared to CON and CON+Ex (p<.05); and DM+Ex group, compared to the CON+Ex group at weeks one, four and eight (p<.05). Tibialis anterior muscle fibers were thicker in the DM+Ex group compared to DM+No Ex, but only at week four (p<.05). Otherwise, no other notable differences were recorded in muscle morphology. [CONCLUSIONS] These results suggest that swimming exercise alone may not be sufficient to induce muscle strength and/or protective effects against muscle atrophy associated with diabetes mellitus. However, this mode of exercise may be considered safe by not compounding the deteriorative effects of this disease.
Abstract
[PURPOSE] The purpose of this study was to assess the effect of swimming exercise in diabetic atrophy by monitoring changes in biomarkers associated with musculoskeletal growth and abnormalities. [METHODS] Ninety-two male Sprague-Dawley rats were randomly divided into four groups: control plus exercise group (CO+Ex), control and no exercise group (CO+No Ex), diabetes plus exercise group (DM+Ex) and diabetes and no exercise group (DM+No Ex). Swimming exercise was implemented for 60 min/day, 5 day/week for a total of eight weeks. Muscle strength and atrophy biomarkers as well as muscle morphology were compared at the first, second, fourth and eighth week of experimentation. [RESULTS] ACE levels were significantly higher in the DM groups (p<.05), however swimming exercise did not significantly affect ACE levels. Irisin levels were significantly higher in the DM and DM+Ex groups compared to the CON, in week one (p<.05), and greater in the DM+Ex group at week two compared to CON+Ex (p<.05), but swimming did not significantly affect irisin levels over the eight-week period in DM rats. In terms of muscle damage, Myl3 expression was unchanged in the CON groups, but significantly higher in the DM+Ex group compared to the CON+Ex group (p<.05). AST was found to be in higher levels in the DM+No Ex group, compared to CON and CON+Ex (p<.05); and DM+Ex group, compared to the CON+Ex group at weeks one, four and eight (p<.05). Tibialis anterior muscle fibers were thicker in the DM+Ex group compared to DM+No Ex, but only at week four (p<.05). Otherwise, no other notable differences were recorded in muscle morphology. [CONCLUSIONS] These results suggest that swimming exercise alone may not be sufficient to induce muscle strength and/or protective effects against muscle atrophy associated with diabetes mellitus. However, this mode of exercise may be considered safe by not compounding the deteriorative effects of this disease.
참고문헌 (55)
- Adams, C. M, "Altered mRNA expression after long‐term soleus electrical stimulation training in humans with paralysis", Muscle & nerve, 43(1), pp.65~75 (2011)
- American Diabetes Association, "Diagnosis and classification of diabetes mellitus", Diabetes care, 29(1), pp.S43~ (2006)
- Amann, B, "ACE inhibitors improve diabetic nephropathy through suppression of renal MCP-1", Diabetes Care, 26(8), pp.2421~2425 (2003)
- Akbarzadeh, A, "Induction of diabetes by streptozotocin in rats", Indian Journal of Clinical Biochemistry, 22(2), pp.60~64 (2007)
- Anastasilakis, A. D, "Circulating irisin in healthy, young individuals: day-night rhythm, effects of food intake and exercise, and associations with gender, physical activity, diet, and body composition", The Journal of Clinical Endocrinology & Metabolism, 99(9), pp.3247~3255 (2014)
- Atlas, S. A, "The renin-angiotensin aldosterone system: Pathophysiological role and pharmacologic inhibition", Journal of managed care pharmacy, 13(8Supp B), pp.9~20 (2007)
- Barzilay, J. I, "Insulin resistance is associated with decreased quadriceps muscle strength in nondiabetic adults aged≥ 70 years", Diabetes care, 32(4), pp.736~738 (2009)
- -dependent myokine that drives brown-fat-like development of white fat and thermogenesis, "Nature", 2012, 463~468
- Brink, M, "Angiotensin II induces skeletal muscle wasting through enhanced protein degradation and down-regulates autocrine insulin-like growth factor I 1", Endocrinology, 142(4), pp.1489~1496 (2001)
- Broderick, T. L, "Exercise training restores abnormal myocardial glucose utilization and cardiac function in diabetes", Diabetes, 2005, pp.21(1), 44~50
- Cameron, N. E, "Angiotensin converting enzyme inhibition prevents development of muscle and nerve dysfunction and stimulates angiogenesis in streptozotocin-diabetic rats", Diabetologia, 35(1), pp.12~18 (1992)
- Chen, N, "Irisin, an exerciseinduced myokine as a metabolic regulator: an updated narrative review", Diabetes, 2016, pp.32(1), 51~59
- Choi, Y. K, "Serum irisin levels in new-onset type 2 diabetes", Diabetes research and clinical practice, 100(1), pp.96~101 (2013)
- Colberg, S. R, "Physical activity", exercise and diabetes: a position statement of the American Diabetes Association, 2016, pp.39(11), 2065~2079
- Emerging Risk Factors Collaboration., "Diabetes mellitus, fasting blood glucose concentration, and risk of vascular disease: a collaborative meta-analysis of 102 prospective studies", The Lancet, 375(9733), pp.2215~2222 (2010)
- Espes, D, "Increased levels of irisin in people with long‐standing Type 1 diabetes", Diabetic Medicine, 32(9), pp.1172~1176 (2015)
- Evans, W. J, "Skeletal muscle loss: cachexia, sarcopenia, and inactivity", The American journal of clinical nutrition, 91(4), pp.1123S~1127S (2010)
- Fukushima, A, "(Pro) renin receptor in skeletal muscle is involved in the development of insulin resistance associated with postinfarct heart failure in mice", American Journal of Physiology-Endocrinology and Metabolism, 307(6), pp.E503~E514 (2014)
- Giboney, P. T, "Mildly elevated liver transaminase levels in the asymptomatic patient", American Family Physician, 71(6), pp.1105~1110 (2005)
- Giannini, E, "Validity and clinical utility of the aspartate aminotransferase–alanine aminotransferase ratio in assessing disease severity and prognosis in patients with hepatitis C virus–related chronic liver disease", Archives of internal medicine, 163(2), pp.218~224 (2003)
- Hart, K. J, "Swim-trained rats have greater bone mass, density, strength, and dynamics", Journal of Applied Physiology, 91, pp.1663~1668 (2001)
- Hepple, R. T, "Muscle atrophy is not always sarcopenia", Journal of Applied Physiology, 113(4), pp.677~679 (2012)
- Junior, M. C, "Response of creatine kinase (CK) levels in diabetics Wistar rats after acute physical exercise", The Journal of exercise and physiology online, 16, pp.99~111 (2013)
- Huh, J. Y, "Exercise-induced irisin secretion is independent of age or fitness level and increased irisin may directly modulate muscle metabolism through AMPK activation", The Journal of Clinical Endocrinology & Metabolism, 99(11), pp.E2154~E2161 (2014)
- Kadoguchi, T, "Angiotensin II can directly induce mitochondrial dysfunction, decrease oxidative fibre number and induce atrophy in mouse hindlimb skeletal muscle", Experimental physiology, 100(3), pp.312~322 (2015)
- Kelley, D. E, "Dysfunction of mitochondria in human skeletal muscle in type 2 diabetes", Diabetes, 51(10), pp.2944~2950 (2002)
- Kistler, K. D, "Physical activity recommendations, exercise intensity, and histological severity of nonalcoholic fatty liver disease", The American journal of gastroenterology, 106(3), pp.460~468 (2011)
- Kuo, C. K, "Inverse association between insulin resistance and gait speed in nondiabetic older men: results from the US National Health and Nutrition Examination Survey (NHANES)1999-2002", Bio Med Central Geriatrics, 9(1), pp.49~ (2009)
- Kurdiova, T, "Effects of obesity, diabetes and exercise on Fndc5 gene expression and irisin release in human skeletal muscle and adipose tissue: in vivo and in vitro studies", The Journal of physiology, 592(5), pp.1091~1107 (2014)
- Youngjeon Lee, "Prophylactic effects of swimming exercise on autophagy-induced muscle atrophy in diabetic rats", Laboratory Animal Research, 28(3), pp.171~179 (2012), 한국실험동물학회
- 이승원, "Appendicular Skeletal Muscle Mass and Insulin Resistance in an Elderly Korean Population: The Korean Social Life, Health and Aging Project-Health Examination Cohort", Diabetes and Metabolism Journal, 39(1), pp.37~45 (2015), 대한당뇨병학회
- Lewis, E. J, "The effect of angiotensin-converting-enzyme inhibition on diabetic nephropathy", New England Journal of Medicine, 329(20), pp.1456~1462 (1993)
- Lindhardt, M, "Proteomic prediction and renin angiotensin aldosterone system inhibition prevention of early diabetic nephRopathy in type 2 diabetic patients with normoalbuminuria (PRIORITY):essential study design and rationale of a randomised clinical multicentre trial", British Medical Journal Open, 6(3), pp.e010310~ (2016)
- Liu, J. J, "Lower circulating irisin is associated with type 2 diabetes mellitus", Journal of Diabetes and its Complications, 27(4), pp.365~369 (2013)
- Liu, J. J, "Relationship between circulating irisin, renal function and body composition in type 2 diabetes. Journal of diabetes and its complications", Journal of diabetes and its complications, 28(2), pp.208~213 (2014)
- Masiello, P, "Experimental NIDDM: development of a new model in adult rats administered streptozotocin and nicotinamide", Diabetes, 47(2), pp.224~229 (1998)
- Moreno-Navarrete, J. M, "Irisin is expressed and produced by human muscle and adipose tissue in association with obesity and insulin resistance", The Journal of Clinical Endocrinology & Metabolism, 98(4), pp.E769~E778 (2013)
- Nathwani, R. A, "Serum alanine aminotransferase in skeletal muscle diseases", Hepatology, 41(2), pp.380~382 (2005)
- Ohta, Y, "Oxidative stress impairs insulin signal in skeletal muscle and causes insulin resistance in postinfarct heart failure", American Journal of Physiology-Heart and Circulatory Physiology, 300(5), pp.H1637~H1644 (2011)
- Pekkala, S, "Are skeletal muscle FNDC5 gene expression and irisin release regulated by exercise and related to health", The Journal of physiology, 591(21), pp.5393~5400 (2013)
- Perry, B. D, "Muscle atrophy in patients with type 2 diabetes mellitus: roles of inflammatory pathways, physical activity and exercise", Exercise Immunology Review, 22, pp.94~108 (2016)
- Robertson, R. P, "Diabetes: strategies to prevent the type 2 diabetes mellitus epidemic", Nature Reviews Endocrinology, 6(3), pp.128~129 (2010)
- Russell, A. P, "Skeletal muscle mitochondria: a major player in exercise, health and disease", Biochimica et Biophysica Acta (BBA)-General Subjects, 1840(4), pp.1276~1284 (2014)
- Semprun-Prieto, L. C, "Angiotensin II induced catabolic effect and muscle atrophy are redox dependent", Biochemical and biophysical research communications, 409(2), pp.217~221 (2011)
- Schiaffino, S, "Developmental myosins: expression patterns and functional significance", Skeletal muscle, 5(1), pp.22~ (2015)
- Sloniger, J. A, "Defective insulin signaling in skeletal muscle of the hypertensive TG (mREN2) 27 rat", American Journal of Physiology-Endocrinology and Metabolism, 288(6), pp.E1074~E1081 (2005)
- Song, Y. H, "Muscle-specific expression of IGF-1 blocks angiotensin II–induced skeletal muscle wasting", The Journal of clinical investigation, 115(2), pp.451~458 (2005)
- Sukhanov, S, "Angiotensin II, oxidative stress and skeletal muscle wasting", The American journal of the medical sciences, 342(2), pp.143~ (2011)
- Tidgren, B, "Renal neurohormonal and vascular responses to dynamic exercise in humans", Journal of Applied Physiology, 70(5), pp.2279~2286 (1991)
- Toledo, F. G, "Effects of physical activity and weight loss on skeletal muscle mitochondria and relationship with glucose control in type 2 diabetes", Diabetes, 56(8), pp.2142~2147 (2007)
- Vozarova, B, "High alanine aminotransferase is associated with decreased hepatic insulin sensitivity and predicts the development of type 2 diabetes", Diabetes, 51(6), pp.1889~1895 (2002)
- Wadén, J, "Leisure-time physical activity and development and progression of diabetic nephropathy in type 1 diabetes: the FinnDiane Study", Diabetologia, 58(5), pp.929~936 (2015)
- Wei, Y, "Angiotensin II-induced NADPH oxidase activation impairs insulin signaling in skeletal muscle cells", Journal of Biological Chemistry, 281(46), pp.35137~35146 (2006)
- Wohaieb, S. A, "Alterations in free radical tissue-defense mechanisms in streptozocin-induced diabetes in rat: effects of insulin treatment", Diabetes, 36(9), pp.1014~1018 (1987)
- Zimmet, P. Z, "Diabetes: a 21st century challenge", The lancet Diabetes & endocrinology, 2(1), pp.56~64 (2014)
