Aim. To assess the plasma leptin responses after exercise stress testing in patients with metabolic syndrome (MS). Material and Methods. We investigated 67 patients with MS, with mean age of years. They underwent exercise stress testing on cycloergometer. The lot was divided into three groups: group 1—10 patients with a true positive test, group 2—18 patients with a true negative test, and group 3—39 patients with a false negative test. Leptin levels were measured using the ELISA method. Results. Leptin levels decreased after effort in patients with MS ( ？ng/mL before and ？ng/mL after the exercise stress test, , ). In groups 1 ( at rest versus ？ng/mL after the exercise test, ) and 3 ( at rest versus ？ng/mL, ), lower leptin levels were recorded immediately after exercise testing. Leptin levels were not significantly lower in group 2 before effort ( ？ng/ml) and after ( ？ng/mL). We found no correlation between leptinemia and exercise stress testing parameters, regardless of group. Conclusion. Our research showed that short-term exercise lowers leptin levels in coronary patients, without a relationship between its parameters and leptin values. 1. Introduction Lately, the adipose tissue was found to be a major endocrine organ which secretes adipokines and cytokines, called adipocytokines. Recent studies have revealed the significant role of adipocytokines in the pathogenesis of obesity, metabolic syndrome, and cardiovascular disease [1]. Thereby, studies performed on humans and animals have shown that adiponectin, apelin, or omentin exerts antiatherogenic effects through various mechanisms, while leptin, resistin, and visfatin are associated with atherosclerosis [1]. So high leptin levels are involved not only in the appearance and progression of atherosclerosis but also in the development of arterial hypertension and metabolic syndrome [1]. The adipose tissue is mainly composed of adipocytes, which produce and release active biopeptides, known as adipokines or adipocytokines. Undoubtedly, adiponectin and leptin are the most widely studied adipokines. Leptin and other proteins, secreted by fat cells or macrophages, are found in large amounts in obese patients, whereas adiponectin levels are low. Recent data shows that adipokines and adipose tissue play a substantial role in the development of obesity, metabolic syndrome, cardiovascular disease, and atherosclerosis process [2–4]. Although the role of adipokines in the pathogenesis of cardiovascular disease is not yet fully understood, there is sufficient evidence that those could be important markers of this
References
[1]
K. G. M. M. Alberti and P. Zimmet, “Metabolic syndrome—a new world-wide definition. A consensus statement from the International Diabetes Federation,” Diabetic Medicine, vol. 23, no. 5, pp. 469–480, 2006.
[2]
H. Wang, W. Luo, and D. T. Eitzman, “Leptin in thrombosis and atherosclerosis,” Current Pharmaceutical Design, 2013.
[3]
V. DeClercq, J. E. Enns, A. Yeganeh, C. G. Taylor, and P. Zahradka, “Modulation of cardiovascular function by adipokines,” Cardiovascular and Hematological Disorders, vol. 13, no. 1, pp. 59–72, 2013.
[4]
H. S. Mattu and H. S. Randeva, “Role of adipokines in cardiovascular disease,” Journal of Endocrinology, vol. 216, no. 1, pp. T17–T36, 2013.
[5]
S. G. Wannamethee, J. Tchernova, P. Whincup et al., “Plasma leptin: associations with metabolic, inflammatory and haemostatic risk factors for cardiovascular disease,” Atherosclerosis, vol. 191, no. 2, pp. 418–426, 2007.
[6]
C. J. Lavie, T. S. Church, R. V. Milani, and C. P. Earnest, “Impact of physical activity, cardiorespiratory fitness, and exercise training on markers of inflammation,” Journal of Cardiopulmonary Rehabilitation and Prevention, vol. 31, no. 3, pp. 137–145, 2011.
[7]
T. H. Luk, Y. L. Dai, C. W. Siu et al., “Effect of exercise training on vascular endothelial function in patients with stable coronary artery disease: a randomized controlled trial,” European Journal of Preventive Cardiology, vol. 19, no. 4, pp. 830–839, 2012.
[8]
D. Zdrenghea, Recuperarea ？i Preven？ia Cardiovascular？, Clusium, Cluj-Napoca, Romania, 2008.
[9]
M. W. Hulver and J. A. Houmard, “Plasma leptin and exercise: recent findings,” Sports Medicine, vol. 33, no. 7, pp. 473–482, 2003.
[10]
R. R. Kraemer, L. G. Johnson, R. Haltom et al., “Serum leptin concentrations in response to acute exercise in postmenopausal women with and without hormone replacement therapy,” Proceedings of the Society for Experimental Biology and Medicine, vol. 221, no. 3, pp. 171–177, 1999.
[11]
L. Pérusse, G. Collier, J. Gagnon et al., “Acute and chronic effects of exercise on leptin levels in humans,” Journal of Applied Physiology, vol. 83, no. 1, pp. 5–10, 1997.
[12]
J. A. Houmard, J. H. Cox, P. S. MacLean, and H. A. Barakat, “Effect of short-term exercise training on leptin and insulin action,” Metabolism: Clinical and Experimental, vol. 49, no. 7, pp. 858–861, 2000.
[13]
A. Leal-Cerro, P. P. Garcia-Luna, R. Astorga et al., “Serum leptin levels in male marathon athletes before and after the marathon run,” Journal of Clinical Endocrinology and Metabolism, vol. 83, no. 7, pp. 2376–2379, 1998.
[14]
M. Landt, G. M. Lawson, J. M. Helgeson et al., “Prolonged exercise decreases serum leptin concentrations,” Metabolism, vol. 46, no. 10, pp. 1109–1112, 1997.
[15]
M. Duclos, J.-B. Corcuff, A. Ruffie, P. Roger, and G. Manier, “Rapid leptin decrease in immediate post-exercise recovery,” Clinical Endocrinology, vol. 50, no. 3, pp. 337–342, 1999.
[16]
J. L. Olive and G. D. Miller, “Differential effects of maximal- and moderate-intensity runs on plasma leptin in healthy trained subjects,” Nutrition, vol. 17, no. 5, pp. 365–369, 2001.
[17]
N. Lakhdar, H. Ben Saad, M. Denguezli et al., “Effects of intense cycling training on plasma leptin and adiponectin and its relation to insulin resistance,” Neuroendocrinology Letters, vol. 34, no. 3, pp. 229–235, 2013.
[18]
O. Ozcelik, H. Celik, A. Ayar, S. Serhatlioglu, and H. Kelestimur, “Investigation of the influence of training status on the relationship between the acute exercise and serum leptin levels in obese females,” Neuroendocrinology Letters, vol. 25, no. 5, pp. 381–385, 2004.
[19]
A. M. Wallace, A. D. McMahon, C. J. Packard et al., “Plasma leptin and the risk of cardiovascular disease in the West of Scotland Coronary Prevention Study (WOSCOPS),” Circulation, vol. 104, pp. 3052–3056, 2001.
[20]
P. Piatti, C. Di Mario, L. D. Monti et al., “Association of insulin resistance, hyperleptinemia, and impaired nitric oxide release with in-stent restenosis in patients undergoing coronary stenting,” Circulation, vol. 108, no. 17, pp. 2074–2081, 2003.
[21]
S. S？derberg, B. Ahrén, B. Stegmayr et al., “Leptin is a risk marker for first-ever hemorrhagic stroke in a population-based cohort,” Stroke, vol. 30, no. 2, pp. 328–337, 1999.
[22]
A. Qasim, N. N. Mehta, M. G. Tadesse et al., “Adipokines, insulin resistance, and coronary artery calcification,” Journal of the American College of Cardiology, vol. 52, no. 3, pp. 231–236, 2008.
[23]
H. Kwon and J. E. Pessin, “Adipokines mediate inflammation and insulin resistance,” Frontiers in Endocrinology, vol. 4, article 71, 2013.
[24]
D. C. W. Lau, B. Dhillon, H. Yan, P. E. Szmitko, and S. Verma, “Adipokines: molecular links between obesity and atheroslcerosis,” American Journal of Physiology—Heart and Circulatory Physiology, vol. 288, no. 5, pp. H2031–H2041, 2005.
[25]
B. Gustafson, “Adipose tissue, inflammation and atherosclerosis,” Journal of Atherosclerosis and Thrombosis, vol. 17, no. 4, pp. 332–341, 2010.
[26]
D. Pop, D. Zdrenghea, L. Stanca, G. Bodisz, D. Petrovai, and B. Borz, “Adiponectin and leptin levels correlate with body mass index and lipid fractions but not with disturbances of glucose metabolism,” Acta Endocrinologica, vol. 5, no. 3, pp. 329–335, 2009.
[27]
C. Iribarren, G. Husson, A. S. Go et al., “Plasma leptin levels and coronary artery calcification in older adults,” Journal of Clinical Endocrinology and Metabolism, vol. 92, no. 2, pp. 729–732, 2007.
[28]
G. F. Fletcher, G. J. Balady, E. A. Amsterdam et al., “Exercise standards for testing and training: a statement for healthcare professionals from the American Heart Association,” Circulation, vol. 104, no. 14, pp. 1694–1740, 2001.
