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Inflammation
Published in: Inflammation 6/2013

01-12-2013

Butyrylcholinesterase and γ-Glutamyltransferase Activities and Oxidative Stress Markers Are Altered in Metabolic Syndrome, But Are Not Affected by Body Mass Index

Authors: Karine S. De Bona, Gabriela Bonfanti, Paula E. R. Bitencourt, Lariane O. Cargnelutti, Priscila S. da Silva, Leidiane De Lucca, Victor C. Pimentel, Etiane Tatsch, Thissiane L. Gonçalves, Melissa Premaor, Rafael N. Moresco, Maria Beatriz Moretto

Published in: Inflammation | Issue 6/2013

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Abstract

Metabolic syndrome (MetS) leads to changes in enzymatic activities, oxidative and inflammatory parameters. Adenosine deaminase (ADA), dipeptidyl peptidase IV (DPP-IV), butyrylcholinesterase (BuChE) and γ-glutamyltransferase (γ-GT) activities, C-reactive protein (hsCRP) and nitric oxide levels (NOx), as well as oxidative stress markers were analyzed in 39 subjects with MetS and 48 controls. Also, the influence of body mass index (BMI) and anthropometric measurements were evaluated. Disturbances in antioxidant defenses and higher γ-GT and BuChE activities, NOx and hsCRP levels were observed in subjects with MetS. These findings remained associated with MetS after adjustment for BMI, except for hsCRP. ADA was correlated with age, insulin levels and HOMA-IR index in MetS. DPP-IV and total cholesterol (TC), BuChE activity and TC, and VIT C and hsCRP levels also were correlated. The analyzed parameters may reflect the inflammatory state of the MetS, and could contribute to prevention and control of various aspects of this syndrome.
Literature
1.
Grundy, S.M., J.I. Cleeman, S.R. Daniels, K.A. Donato, R.H. Eckel, B.A. Franklin, D.J. Gordon, R.M. Krauss, P.J. Savage, S.C. Jr Smith, J.A. Spertus, and F. Costa. 2005. American Heart Association; National Heart, Lung, and Blood Institute, Diagnosis and management of the metabolic syndrome: an American Heart Association/National Heart, Lung, and Blood Institute Scientific Statement. Circulation 112: 2735–2752.PubMedCrossRef
2.
Phillips, C., J. Lopez-Miranda, F. Perez-Jimenez, R. McManus, and H.M. Roche. 2006. Genetic and nutrient determinants of the metabolic syndrome. Current Opinion in Cardiology 21: 185–193.PubMedCrossRef
3.
Batsis, J.A., R.E. Nieto-Martinez, and F. Lopez-Jimenez. 2007. Metabolic syndrome: from global epidemiology to individualized medicine. Clinical Pharmacology and Therapeutics 82: 509–524.PubMedCrossRef
4.
Marquezine, G.F., C.M. Oliveira, A.C. Pereira, J.E. Krieger, and J.G. Mill. 2008. Metabolic syndrome determinants in an urban population from Brazil: social class and gender-specific interaction. International Journal of Cardiology 129: 259–265.PubMedCrossRef
5.
Kuno, M., N. Seki, S. Tsujimoto, I. Nakanishi, T. Kinoshita, K. Nakamura, T. Terasaka, N. Nishio, A. Sato, and T. Fujii. 2006. Anti-inflammatory activity of non-nucleoside adenosine deaminase inhibitor FR234938. European Journal of Pharmacology 534: 241–249.PubMedCrossRef
6.
Conlon, B.A., and W.R. Law. 2004. Macrophages are a source of extracellular adenosine deaminase-2 during inflammatory responses. Clinical and Experimental Immunology 138: 14–20.PubMedCrossRef
7.
Prakash, M.S., S. Chennaiah, Y.S.R. Murthy, E. Anjaiah, S. Ananda Rao, and C. Suresh. 2006. Altered adenosine deaminase activity in type 2 diabetes mellitus. Journal Indian Academy of Clinical Medicine 7: 114–117.
8.
Bopp, A., K.S. De Bona, L.P. Bellé, R.N. Moresco, and M.B. Moretto. 2009. Syzygium cumini inhibits adenosine deaminase activity and reduces glucose levels in hyperglycemic patients. Fundamental and Clinical Pharmacology 23: 501–507.PubMedCrossRef
9.
Kurtul, N., S. Pence, E. Akarsu, H. Kocoglu, Y. Aksoy, and H. Aksoy. 2004. Adenosine deaminase activity in the serum of type 2 diabetic patients. Acta Médica 47: 33–35.PubMed
10.
Dong, R.P., J. Kameoka, M. Hegen, T. Tanaka, Y. Xu, S.F. Schlossman, and C. Morimoto. 1996. Characterization of adenosine deaminase binding to human CD26 on T cells and its biologic role in immune response. The Journal of Immunology 156: 1349–1355.PubMed
11.
Stancíková, M., Z. Lojda, J. Lukác, and M. Ruzicková. 1992. Dipeptidyl peptidase IV in patients with systemic lupus erythematosus. Clinical and Experimental Rheumatology 10: 381–385.PubMed
12.
Lugari, R., A. Dei Cas, D. Ugolotti, A.L. Barilli, C. Camellini, G.C. Ganzerla, A. Luciani, B. Salerni, F. Mittenperger, S. Nodari, A. Gnudi, and R. Zandomeneghi. 2004. Glucagon-like peptide 1 (GLP-1) secretion and plasma dipeptidyl peptidase IV (DPP-IV) activity in morbidly obese patients undergoing biliopancreatic diversion. Hormone and Metabolism Research 36: 111–115.CrossRef
13.
Ryskjaer, J., C.F. Deacon, R.D. Carr, T. Krarup, S. Madsbad, J. Holst, and T. Vilsbøll. 2006. Plasma dipeptidyl peptidase-IV activity in patients with type-2 diabetes mellitus correlates positively with HbAlc levels, but is not acutely affected by food intake. European Journal of Endocrinology 155: 485–493.PubMedCrossRef
14.
De Bona, K.S., G. Bonfanti, L.O. Cargnelutti, P.E. Bitencourt, P.S. da Silva, R. Ceolin, V.C. Pimentel, and M.B. Moretto. 2012. Lymphocytic enzymes and lipid peroxidation in patients with metabolic syndrome. Clinical Biochemistry 45: 1081–1085.PubMedCrossRef
15.
Randell, E.W., M.S. Mathews, H. Zhang, J.S. Seraj, and G. Sun. 2005. Relationship between serum butyrylcholinesterase and the metabolic syndrome. Clinical Biochemistry 38: 799–805.PubMedCrossRef
16.
Abbott, C.A., M.I. Mackness, S. Kumar, A.O. Olukoga, C. Gordon, S. Arrol, D. Bhatnagar, A.J. Boulton, and P.N. Durrington. 1993. Relationship between serum butyrylcholinesterase activity, hypertriglyceridaemia and insulin sensitivity in diabetes mellitus. Clinical Science 85: 77–81.PubMed
17.
Alcantara, V.M., E.A. Chautard-Freire-Maia, M. Scartezini, M.S. Cerci, K. Braun-Prado, and G. Picheth. 2002. Butyrylcholinesterase activity and risk factors for coronary artery disease. Scandinavian Journal of Clinical and Laboratory Investigation 62: 399–404.PubMedCrossRef
18.
Vaidya, D., M. Szklo, M. Cushman, P. Holvoet, J. Polak, H. Bahrami, N.S. Jenny, and P. Ouyang. 2011. Association of endothelial and oxidative stress with metabolic syndrome and subclinical atherosclerosis: multi-ethnic study of atherosclerosis. European Journal of Clinical Nutrition 65: 818–825.PubMedCrossRef
19.
Sun, Y.X., S.J. Hu, X.H. Zhang, J. Sun, C.H. Zhu, and Z.J. Zhang. 2006. Plasma levels of vWF and NO in patients with metabolic syndrome and their relationship with metabolic disorders. Zhejiang Da Xue Xue Bao. Yi Xue Ban 35: 315–318.PubMed
20.
Zahedi Asl, S., A. Ghasemi, and F. Azizi. 2008. Serum nitric oxide metabolites in subjects with metabolic syndrome. Clinical Biochemistry 41: 1342–1347.PubMedCrossRef
21.
Koh, K.K., M.J. Quon, S.H. Han, W.J. Chung, J.A. Kim, and E.K. Shin. 2006. Vascular and metabolic effects of candesartan: insights from therapeutic interventions. Journal of Hypertension. Supplement 24: 31–38.CrossRef
22.
Assumpção, C.R., T.M.C. Brunini, C. Matsuura, A.C. Resende, and A.C. Mendes- Ribeiro. 2008. Impact of the l-arginine-nitric oxide pathway and oxidative stress on the pathogenesis of the metabolic syndrome. Open Biochemistry Journal 2: 108–115.CrossRef
23.
Friedewald, W.T., R.I. Levy, and D.S. Fredrickson. 1972. Estimation of concentration of low-density lipoprotein in plasma, without use of preparative ultracentrifuge. Clinical Chemistry 18: 499–502.PubMed
24.
Matthews, D.R., J.P. Hosker, A.S. Rudenski, B.A. Naylor, D.F. Treacher, and R.C. Turner. 1985. Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia 28: 412–419.PubMedCrossRef
25.
Giusti, G., and C. Gakis. 1971. Temperature conversion factors, activation energy, relative substrate specificity and optimum pH of adenosine deaminase from human serum and tissues. Enzyme 12: 417–425.PubMed
26.
Jarmołowska, B., K. Bielikowicz, M. Iwan, K. Sidor, E. Kostyra, and M. Kaczmarski. 2007. Serum activity of dipeptidyl peptidase IV (DPPIV; EC 3.4.14.5) in breast-fed infants with symptoms of allergy. Peptides 28: 678–682.PubMedCrossRef
27.
Ellman, G.C., K.D. Courtney, V. Andres, and R.M. Feather- Stone. 1961. A new and rapid colorimetric determination of acetylcholinesterase activity. Biochemical Pharmacology 7: 88–95.PubMedCrossRef
28.
Tatsch, E., G.V. Bochi, S. Pereira Rda, H. Kober, V.A. Agertt, M.M. de Campos, P. Gomes, M.M. Duarte, and R.N. Moresco. 2011. A simple and inexpensive automated technique for measurement of serum nitrite/nitrate. Clinical Biochemistry 44: 348–350.PubMedCrossRef
29.
Boyne, A.F., and G.L. Ellman. 1972. A methodology for analysis of tissue sulfhydryl components. Analytical Biochemistry 46: 639–653.PubMedCrossRef
30.
Jacqes-Silva, M.C., C.W. Nogueira, L.C. Broch, E.M. Flores, and J.B. Rocha. 2001. Diphenyl diselenide and ascorbic acid changes deposition of selenium and brain of mice. Phamacology and Toxicology 88: 119–125.CrossRef
31.
Galley, H., M.J. Davies, and N.R. Webster. 1996. Ascorbil radical formation in patients with sepsis: effects of ascorbate loading. Free Radical Biology and Medicine 20: 139–143.PubMedCrossRef
32.
Lapenna, D., G. Ciofani, S.D. Pierdomenico, M.A. Giamberardino, and F. Cuccurullo. 2001. Reaction conditions affecting the relationship between thiobarbituric acid reactivity and lipid peroxides in human plasma. Free Radical Biology and Medicine 31: 331–335.PubMedCrossRef
33.
Festa, A., R. D'Agostino Jr., G. Howard, L. Mykkänen, R.P. Tracy, and S.M. Haffner. 2000. Chronic subclinical inflammation as part of the insulin resistance syndrome: the Insulin Resistance Atherosclerosis Study (IRAS). Circulation 102: 42–47.PubMedCrossRef
34.
Ridker, P.M., J.E. Buring, N.R. Cook, and N. Rifai. 2003. C-Reactive protein, the metabolic syndrome, and risk of incident cardiovascular events: an 8-year follow-up of 14 719 initially healthy American women. Circulation 107: 391–397.PubMedCrossRef
35.
Haas, M.J., and A.D. Mooradian. 2011. Inflammation, high-density lipoprotein and cardiovascular dysfunction. Current Opinion in Infectious Diseases 24: 265–272.PubMedCrossRef
36.
Elks, C.M., and J. Francis. 2010. Central adiposity, systemic inflammation, and the metabolic syndrome. Current Hypertension Reports 12: 99–104.PubMedCrossRef
37.
Magarian, E.O., and A.J. Dietz. 1987. Correlation of cholinesterase with serum lipids and lipoproteins. The Journal of Clinical Pharmacology 27: 819–820.CrossRef
38.
Sridhar, G.R., G. Nirmala, A. Apparao, A.S. Madhavi, S. Sreelatha, J.S. Rani, and P. Vijayalakshmi. 2005. Serum butyrylcholinesterase in type 2 diabetes mellitus: a biochemical and bioinformatics approach. Lipids in Health and Disease 8: 4–18.
39.
Kalman, J., A. Juhasz, Z. Rakonczay, G. Abrahám, M. Zana, K. Boda, T. Farkas, B. Penke, and Z. Janka. 2004. Increase serum butyrylcholinesterase activity in type IIb hyperlipidemic patients. Life Science 75: 1195–1204.CrossRef
40.
Meghji, P. 1991. Adenosine production and metabolism. In Adenosine in the nervous system, ed. T. Stone, 25–42. London: Academic.CrossRef
41.
Rosenstock, J., M.A. Baron, S. Dejager, D. Mills, and A. Schweizer. 2007. Comparison of vildagliptin and rosiglitazone monotherapy in patients with type 2 diabetes: a 24-week, double-blind, randomized trial. Diabetes Care 30: 217–223.PubMedCrossRef
42.
Bozbaş, H., A. Yıldırır, E. Karaçağlar, O. Demir, T. Ulus, S. Eroğlu, A. Aydınalp, B. Ozin, and H. Müderrisoğlu. 2011. Increased serum gamma glutamyltransferase activity in patients with metabolic syndrome. Türk Kardiyoloji Derneği Arşivi 39: 122–128.PubMedCrossRef
43.
Giral, P., N. Jacob, C. Dourmap, B. Hansel, A. Carrié, E. Bruckert, X. Girerd, and M.J. Chapman. 2008. Elevated gamma-glutamyltransferase activity and perturbed thiol profile are associated with features of metabolic syndrome. Arteriosclerosis, Thrombosis, and Vascular Biology 28: 587–593.PubMedCrossRef
44.
Vincent, H.K., and A.G. Taylor. 2006. Biomarkers and potential mechanisms of obesity-induced oxidant stress in humans. International Journal of Obesity (Lond) 30: 400–418.CrossRef
45.
Doi, Y., Y. Kiyohara, M. Kubo, T. Ninomiya, Y. Wakugawa, K. Yonemoto, M. Iwase, and M. Iida. 2005. Elevated C-reactive protein is a predictor of diabetes in a general Japanese population: the Hisayama study. Diabetes Care 28: 2497–2500.PubMedCrossRef
46.
Ford, E.S. 2003. The metabolic syndrome and C-reactive protein, fibrinogen, and leukocyte count: findings from the Third National Health and Nutrition Examination Survey. Atherosclerosis 168: 351–358.PubMedCrossRef
47.
Amiri, F. 2009. Metabolic syndrome, insulin resistance and oxidative stress: adding insights to improve cardiovascular prevention. Journal of Hypertension 27: 1352–1354.PubMedCrossRef
48.
Pischon, T., F.B. Hu, K.M. Rexrode, J.C. Girman, A.E. Manson, and E.B. Rimm. 2008. Inflammation, the metabolic syndrome, and risk of coronary heart disease in women and men. Atherosclerosis 197: 392–399.PubMedCrossRef
Metadata
Title
Butyrylcholinesterase and γ-Glutamyltransferase Activities and Oxidative Stress Markers Are Altered in Metabolic Syndrome, But Are Not Affected by Body Mass Index
Authors
Karine S. De Bona
Gabriela Bonfanti
Paula E. R. Bitencourt
Lariane O. Cargnelutti
Priscila S. da Silva
Leidiane De Lucca
Victor C. Pimentel
Etiane Tatsch
Thissiane L. Gonçalves
Melissa Premaor
Rafael N. Moresco
Maria Beatriz Moretto
Publication date
01-12-2013
Publisher
Springer US
Published in
Inflammation / Issue 6/2013
Print ISSN: 0360-3997
Electronic ISSN: 1573-2576
DOI
https://doi.org/10.1007/s10753-013-9697-9

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