Lower Serum Paraoxonase-1 Activity Is Related to Higher Serum Amyloid A Levels in Metabolic Syndrome

Archives of Medical Research

Volumn 42, Issue 3, 2011, Pages 219-225

  Kappelle, Paul Jan Willem Herman ^a   Bijzet, Johan ^a   Hazenberg, Bouke Pier ^a   Dullaart, Robin Pieter Frank ^a  

^a UNIVERSITY MEDICAL CENTER GRONINGEN   (Netherlands)

Author keywords

C reactive protein; High density lipoprotein function; Metabolic syndrome; Paraoxonase 1 activity; Serum amyloid A

Indexed keywords

APOLIPOPROTEIN; APOLIPOPROTEIN A1; ARYLDIALKYLPHOSPHATASE 1; C REACTIVE PROTEIN; HIGH DENSITY LIPOPROTEIN CHOLESTEROL; SERUM AMYLOID A; TRIACYLGLYCEROL;

ADULT; AGED; ANTIOXIDANT ACTIVITY; ARTICLE; CLINICAL ARTICLE; CONTROLLED STUDY; ENZYME ACTIVITY; ENZYME BLOOD LEVEL; FEMALE; HUMAN; INSULIN RESISTANCE; LIPOPROTEIN BLOOD LEVEL; MALE; METABOLIC SYNDROME X; PROTEIN BLOOD LEVEL; SEX DIFFERENCE;

AGED; ARYLDIALKYLPHOSPHATASE; C-REACTIVE PROTEIN; CASE-CONTROL STUDIES; CHOLESTEROL; FEMALE; HUMANS; LINEAR MODELS; LIPOPROTEINS, HDL; MALE; METABOLIC SYNDROME X; MIDDLE AGED; SERUM AMYLOID A PROTEIN;

EID: 79959697104     PISSN: 01884409     EISSN: 18735487     Source Type: Journal    
DOI: 10.1016/j.arcmed.2011.05.002     Document Type: Article

References (46)

1. Vega G.L., Grundy S.M. Hypoalphalipoproteinemia (low high density lipoprotein cholesterol) as a risk factor for coronary heart disease. Curr Opin Lipidol 1996, 7:209-216.
2. Major Lipids, Apolipoproteins, and Risk of Vascular Disease. JAMA 2009, 302:1993-2000. The Emerging Risk Factors Collaboration.
3. Borggreve S.E., de Vries R., Dullaart R.P.F. Alterations in high-density lipoprotein metabolism and reverse cholesterol transport in insulin resistance and type 2 diabetes mellitus: role of lipolytic enzymes, lecithin:cholesterol acyltransferase and lipid transfer proteins. Eur J Clin Invest 2003, 33:1051-1069.
4. Linsel-Nitschke P., Tall A.R. HDL as a target in the treatment of atherosclerotic cardiovascular disease. Nat Rev Drug Discovery 2005, 4:193-205.
5. Kontush A., Chapman M.J. Functionally defective high-density lipoprotein: a new therapeutic target at the crossroads of dyslipidemia, inflammation, and atherosclerosis. Pharmacol Rev 2006, 58:342-374.
6. de Goma E.M., de Goma R.L., Rader D.J. Beyond high-density lipoprotein cholesterol levels evaluating high-density lipoprotein function as influenced by novel therapeutic approaches. J Am Coll Cardiol 2008, 51:2199-2211.
7. Dullaart R.P.F., Perton F., Kappelle P.J., et al. Plasma lecithin:cholesterol acyltransferase activity modifies the inverse relationship of C-reactive protein with HDL cholesterol in nondiabetic men. Biochim Biophys Acta 2010, 1801:84-88.
8. Singh I.M., Shishehbor M.H., Ansell B.J. High-density lipoprotein as a therapeutic target. JAMA 2007, 298:786-798.
9. Navab M., Anantharamaiah G.M., Reddy S.T., et al. HDL as a biomarker, potential therapeutic target, and therapy. Diabetes 2009, 58:2711-2717.
10. Kappelle P.J., van Tol A., Wolffenbuttel B.H.R., et al. Cholesteryl ester transfer protein inhibition in cardiovascular risk management: ongoing trials will end the confusion. Cardiovasc Ther 2010, Epub ahead of print; PMID: 20645987.
11. Corsetti J.P., Gansevoort R.T., Sparks C.E., et al. Inflammation reduces HDL protection against primary cardiac risk. Eur J Clin Invest 2010, 40:483-489.
12. Mackness B., Davies G.K., Turkie W., et al. Paraoxonase status in coronary heart disease. Are activity and concentration more important than genotype?. Arterioscler Thromb Vasc Biol 2001, 21:1451-1457.
13. Deakin S.P., James R.W. Genetic and environmental factors modulating serum concentrations and activities of the antioxidant enzyme paraoxonase-1. Clin Sci 2004, 107:435-447.
14. Mackness B., Quarck R., Verreth W., et al. Human paraoxonase-1 overexpression inhibits atherosclerosis in a mouse model of metabolic syndrome. Arterioscler Thromb Vasc Biol 2006, 26:1545-1550.
15. Granér M., James R.W., Kahri J., et al. Association of paraoxonase-1 activity and concentration with angiographic severity and extent of coronary artery disease. J Am Coll Cardiol 2006, 47:2429-2435.
16. Ridker P.M., Hennekens C.H., Buring J.E., et al. C-reactive protein and other markers of inflammation in the prediction of cardiovascular disease in women. N Engl J Med 2000, 342:836-843.
17. Johnson B.D., Kip K.E., Marroquin O.C., et al. National Heart, Lung, and Blood Institute. Serum amyloid A as a predictor of coronary artery disease and cardiovascular outcome in women: the National Heart, Lung, and Blood Institute-Sponsored Women's Ischemia Syndrome Evaluation (WISE). Circulation 2004, 109:726-732.
18. Danesh J., Whincup P., Walker M., et al. Low grade inflammation and coronary heart disease: prospective study and updated meta-analyses. BMJ 2000, 321:199-204.
19. Chait A., Han C.Y., Oram J.F., et al. Lipoprotein-associated inflammatory proteins: markers or mediators of cardiovascular disease?. J Lipid Res 2005, 46:389-403.
20. Jacobs M., van Greevenbroek M.M., van der Kallen C.J., et al. Low-grade inflammation can partly explain the association between the metabolic syndrome and either coronary artery disease or severity of peripheral arterial disease: the CODAM study. Eur J Clin Invest 2009, 39:437-444.
21. Jylhävä J., Haarala A., Eklund C., et al. Serum amyloid A is independently associated with metabolic risk factors but not with early atherosclerosis: the Cardiovascular Risk in Young Finns Study. J Intern Med 2009, 266:286-295.
22. Dullaart R.P.F., de Vries R., Dallinga-Thie G.M., et al. Phospholipid transfer protein activity is determined by type 2 diabetes mellitus and metabolic syndrome, and is positively associated with serum transaminases. Clin Endocrinol 2008, 68:375-381.
23. Mackness B., Hine D., McElduff P., et al. High C-reactive protein and low paraoxonase1 in diabetes as risk factors for coronary heart disease. Atherosclerosis 2006, 186:396-401.
24. Dullaart R.P.F., de Vries R., Sluiter W.J., et al. High plasma C-reactive protein (CRP) is related to low paraoxonase-i (PON-I) activity independently of high leptin and low adiponectin in type 2 diabetes mellitus. Clin Endocrinol 2009, 70:221-226.
25. Sentí M., Tomás M., Fitó M., et al. Antioxidant paraoxonase 1 activity in the metabolic syndrome. J Clin Endocrinol Metab 2003, 88:5422-5426.
26. Garin M.C., Kalix B., Morabia A., et al. Small, dense lipoprotein particles and reduced paraoxonase-1 in patients with the metabolic syndrome. J Clin Endocrinol Metab 2005, 90:2264-2269.
27. Coetzee G.A., Strachan A.F., van der Westhuyzen D.R., et al. Serum amyloid A-containing human high density lipoprotein 3. Density, size, and apolipoprotein composition. J Biol Chem 1986, 261:9644-9651.
28. James R.W., Deakin S.P. The importance of high-density lipoproteins for paraoxonase-1 secretion, stability, and activity. Free Radic Biol Med 2004, 37:1986-1994.
29. Cabana V.G., Reardon C.A., Feng N., et al. Serum paraoxonase: effect of the apolipoprotein composition of HDL and the acute phase response. J Lipid Res 2003, 44:780-792.
30. Gaidukov L., Tawfik D.S. High affinity, stability, and lactonase activity of serum paraoxonase PON1 anchored on HDL with ApoA-I. Biochemistry 2005, 44:11843-11854.
31. Han C.Y., Chiba T., Campbell J.S., et al. Reciprocal and coordinate regulation of serum amyloid A versus apolipoprotein A-I and paraoxonase-1 by inflammation in murine hepatocytes. Arterioscler Thromb Vasc Biol 2006, 26:1806-1813.
32. Van Lenten B.J., Hama S.Y., de Beer F.C., et al. Anti-inflammatory HDL becomes pro-inflammatory during the acute phase response. Loss of protective effect of HDL against LDL oxidation in aortic wall cell cocultures. J Clin Invest 1995, 96:2758-2767.
33. Stuveling E.M., Hillege H.L., Bakker S.J., et al. PREVEND study group. C-reactive protein and microalbuminuria differ in their associations with various domains of vascular disease. Atherosclerosis 2004, 172:107-114.
34. Grundy S.M., Cleeman J.I., Daniels S.R., et al. Diagnosis and management of the metabolic syndrome: an American Heart Association/National Heart, Lung and Blood Institute Scientific Statement. Circulation 2005, 112:2735-2752.
35. Van Himbergen T.M., Roest M., de Graaf J., et al. Indications that paraoxonase-1 contributes to plasma high density lipoprotein levels in familial hypercholesterolemia. J Lipid Res 2005, 46:445-451.
36. Hazenberg B.P., Limburg P.C., Bijzet J., et al. A quantitative method for detecting deposits of amyloid A protein in aspirated fat tissue of patients with arthritis. Ann Rheum Dis 1999, 58:96-102.
37. Watson A.D., Berliner J.A., Hama S.Y., et al. Protective effect of high density lipoprotein associated paraoxonase. Inhibition of the biological activity of minimally oxidized low density lipoprotein. J Clin Invest 1995, 96:2882-2891.
38. Deakin S., Moren X., James R.W. HDL oxidation compromises its influence on paraoxonase-1 secretion and its capacity to modulate enzyme activity. Arterioscler Thromb Vasc Biol 2007, 27:1146-1152.
39. de Beer M.C., Webb N.R., Wroblewski J.M., et al. Impact of serum amyloid A on high density lipoprotein composition and levels. J Lipid Res 2010, PMID: 20667817; Epub ahead of print.
40. Lagos K.G., Filippatos T.D., Tsimihodimos V., et al. Alterations in the high density lipoprotein phenotype and HDL-associated enzymes in subjects with metabolic syndrome. Lipids 2009, 44:9-16.
41. Tabur S., Torun A.N., Sabuncu T., et al. Non-diabetic metabolic syndrome and obesity do not affect serum paraoxonase and arylesterase activities but do affect oxidative stress and inflammation. Eur J Endocrinol 2010, 162:535-541.
42. Roest M., van Himbergen T.M., Barendrecht A.B., Peeters P.H., et al. Genetic and environmental determinants of the PON-1 phenotype. Eur J Clin Invest 2007, 37:187-196.
43. Hedrick C.C., Thorpe S.R., Fu M.X., et al. Glycation impairs high-density lipoprotein function. Diabetologia 2000, 43:312-320.
44. Nobécourt E., Tabet F., Lambert G., et al. Nonenzymatic glycation impairs the antiinflammatory properties of apolipoprotein A-I. Arterioscler Thromb Vasc Biol 2010, 30:766-772.
45. Bos M.B., de Vries J.H., Wolffenbuttel B.H., et al. The prevalence of the metabolic syndrome in the Netherlands: increased risk of cardiovascular diseases and diabetes mellitus type 2 in one quarter of persons under 60. Ned Tijdschr Geneesk 2007, 151:2382-2388.
46. Kontush A., de Faria E.C., Chantepie S., et al. A normotriglyceridemic, low HDL-cholesterol phenotype is characterised by elevated oxidative stress and HDL particles with attenuated antioxidative activity. Atherosclerosis 2005, 2:277-285.