Acta Medica Iranica 2015. 53(1):25-29.

Association between adipokine and myeloperoxidase levels in patients with coronary artery disease.
Gholam Basati, Amirnader Emami Razavi, Soheila Abdi, Nizal Sarrafzadegan

Abstract


The adipokines, leptin and adiponectin, have a prominent role in the pathogenesis of coronary artery disease (CAD). The inflammatory enzyme, myeloperoxidase (MPO) also has an important role in the pathogenesis of CAD. Association of the adipokines with MPO remains to be resolved in patients with CAD. In this case-control study, 100 patients with CAD and 100 control subjects were appropriately recruited. Angiographic evaluation assigned the presence of CAD. Plasma leptin, adiponectin and MPO concentrations were measured using immunoassay methods. Other conventional cardiovascular risk factors were also recorded. Leptin and MPO concentrations were significantly increased in CAD patients compared to control subjects (25.38 ± 5.91 ng/ml vs. 3.68 ± 1.95 ng/mL and 52.85 ± 12.90 ng/mL vs.  23.00 ± 3.60 ng/mL, P=0.001, respectively). In contrast, adiponectin was significantly decreased in CAD patients compared to control subjects (5.62 ± 1.15 µg/mL vs. 9.25 ± 1.8, P = 0.001). There was a strong positive association between leptin and MPO concentrations only in CAD patients (P = 0.01). In contrast, a significant inverse association was found between adiponectin and MPO concentrations in CAD patients (P = 0.01). The associations also were significant after adjustment for other conventional risk factors (P = 0.001). Considering the presence of significant association between leptin and MPO, as well as adiponectin and MPO in patients with CAD, it may be inferred that the contribution of the adipokines in the pathogenesis of CAD may be, in part, through affecting the MPO concentration.

Keywords


Adipokines; CAD pathogenesis; Leptin; Myeloperoxidase

Full Text:

PDF

References


Calabrò P GE, Maddaloni V, Malvezzi M, et al. Adipose tissue-mediated inflammation: the missing link between obesity and cardiovascular disease? Intern Emerg Med 2009;4(1):25-34.

Guzik TJ MD, Korbut R. Adipocytokines - a novel link between inflammation and vascular function? J Physiol Pharmacol 2006;57(4):505-28.

Berg AH, Scherer PE. Adipose tissue, inflammation, and cardiovascular disease. Circ Res 2005;96(9):939-49.

Hara T, Fujiwara H, Shoji T, et al. Decreased plasma adiponectin levels in young obese males. J Atheroscler Thromb 2003;10(4):234-8.

Ikeoka D, Mader JK, Pieber TR. Adipose tissue, inflammation and cardiovascular disease. Revi Assoc Méd Bras 2010;56(1):116-21.

Broedl UC, Lebherz C, Lehrke M, et al. Low adiponectin levels are an independent predictor of mixed and noncalcified coronary atherosclerotic plaques. PLoS One 2009;4(3):e4733.

Basati G, Pourfarzam M, Movahedian A, et al. Reduced plasma adiponectin levels relative to oxidized low density lipoprotein and nitric oxide in coronary artery disease patients. Clinics (Sao Paulo) 2011;66(7):1129-35.

Wallace AM, McMahon AD, Packard CJ, et al. Plasma leptin and the risk of cardiovascular disease in the west of Scotland coronary prevention study (WOSCOPS). Circulation 2001;104(25):3052-6.

Dubey L, Zeng HS, Wang HJ, et al. Potential role of adipocytokine leptin in acute coronary syndrome. Asian Cardiovasc Thorac Ann 2008;16(2):124-8.

Wolk R, Berger P, Lennon RJ, et al. Plasma leptin and prognosis in patients with established coronary atherosclerosis. J Am Coll Cardiol 2004;44(9):1819-24.

Lago F, Gómez R, Gómez-Reino JJ, et al. Adipokines as novel modulators of lipid metabolism. Trends Biocheml Sci 2009;34(10):500-10.

Nicholls SJ, Hazen SL. Myeloperoxidase and cardiovascular disease. Arterioscler Thromb Vasc Biol 2005;25(6):1102-11.

Stocker R, Keaney JF Jr. Role of oxidative modifications in atherosclerosis. Physiol Rev 2004;84(4):1381-478.

Carr AC, McCall MR, Frei B. Oxidation of LDL by Myeloperoxidase and Reactive Nitrogen Species: Reaction Pathways and Antioxidant Protection. Arterioscler Thromb Vasc Biol 2000;20(7):1716-23.

Abu-Soud HM, Hazen SL. Nitric oxide is a physiological substrate for mammalian peroxidases. J Biol Chem 2000;275(48):37524-32.

Xu J, Xie Z, Reece R, et al. Uncoupling of Endothelial Nitric Oxidase Synthase by Hypochlorous Acid: Role of NAD(P)H Oxidase–Derived Superoxide and Peroxynitrite. Arterioscler Thromb Vasc Biol 2006;26(12):2688-95.

Dolezalova R, Haluzik MM, Bosanska L, et al. Effect of PPAR-gamma agonist treatment on markers of endothelial dysfunction in patients with type 2 diabetes mellitus. Physiol Res 2007;56(6):741-8.

Barbier M, Cherbut C, Aube A, et al. Elevated plasma leptin concentrations in early stages of experimental intestinal inflammation in rats. Gut 1998;43(6):783-90.

Beltowski J. Leptin and atherosclerosis. Atherosclerosis 2006;189(1):47-60.

Martin SS, Qasim A, Reilly MP. Leptin Resistance. A Possible Interface of Inflammation and Metabolism in Obesity-Related Cardiovascular Disease. J Am Coll Cardiol 2008;52(15):1201-10.

La Cava A, Matarese G. The weight of leptin in immunity. Nat Rev Immunol 2004;4(5):371-9.

Sanchez Margalet V, Martin Romero C, Santos Alvarez J, et al. Role of leptin as an immunomodulator of blood mononuclear cells: mechanisms of action. Clin Exp Immunol 2003;133(1):11-9.

Singh U, Devaraj S, Jialal I. C-reactive protein stimulates myeloperoxidase release from polymorphonuclear cells and monocytes: implications for acute coronary syndromes. Clin Chem 2009;55(2):361-4.

Shimada K, Miyazaki T, Daida H. Adiponectin and atherosclerotic disease. Clin Chim Acta 2004;344(1-2):1-12.

Abd El Maksoud H, Gindi RR, Abdel-Nabi YM. Adiponectin and yeloperoxydase in acutemyocardial infarction individuals. BVMJ-SE 2011;7(2):109-15.

Yokota T, Oritani K, Takahashi I, et al. Adiponectin, a new member of the family of soluble defense collagens, negatively regulates the growth of myelomonocytic progenitors and the functions of macrophages. Blood 2000;96(5):1723-32.


Refbacks

  • There are currently no refbacks.


Creative Commons Attribution-NonCommercial 3.0

This work is licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License which allows users to read, copy, distribute and make derivative works for non-commercial purposes from the material, as long as the author of the original work is cited properly.