Postchallenge responses of nitrotyrosine and TNF-alpha during 75-g oral glucose tolerance test are associated with the presence of coronary artery diseases in patients with prediabetes

Springer Science and Business Media LLC - Tập 11 - Trang 1-11 - 2012
Chih-Sheng Chu1,2,3,4, Kun-Tai Lee1,2, Kai-Hong Cheng1,2,4, Min-Yi Lee4, Hsuan-Fu Kuo3,4, Tsung-Hsien Lin1,2, Ho-Ming Su1,2, Wen-Chol Voon1,2, Sheng-Hsiung Sheu1,2, Wen-Ter Lai1,2
1Division of Cardiology, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan
2Department of Internal Medicine, Faculty of Medicine, College of Medicine, Kaohsiung, Taiwan
3Department of Internal Medicine, Kaohsiung Municipal Ta-Tung Hospital, Kaohsiung, Taiwan
4Graduate Institute of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan

Tóm tắt

Meta-analysis has demonstrated an exponential relationship between 2-hr postchallenge hyperglycemia and coronary artery disease (CAD). Pulsatile hyperglycemia can acutely increase proinflammatory cytokines by oxidative stress. We hypothesized that postchallenge proinflammatory and nitrosative responses after 75 g oral glucose tolerance tests (75 g-OGTT) might be associated with CAD in patients without previously recognized type 2 diabetes mellitus (T2DM). Serial changes of plasma glucose (PG), tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6) and nitrotyrosine levels were analyzed during 75 g-OGTT in 120 patients (81 male; age 62 ± 11 years) before coronary angiography. Patients were classified as normal (NGT; 42%), impaired (IGT; 34%) and diabetic (T2DM; 24%) glucose tolerance by 75 g-OGTT. Postchallenge hyperglycemia elicited TNF-α, IL-6 and nitrotyrosine levels time-dependently, and 2-hr median levels of TNF-α (7.1 versus 6.4 pg/ml; P < 0.05) and nitrotyrosine (1.01 versus 0.83 μ mol/l; P < 0.05), but not IL-6 or PG, were significantly higher in patients with CAD in either IGT or T2DM groups. After adjusting risk factors and glucose tolerance status, 2-hr nitrotyrosine in highest quartiles (OR: 3.1, P < 0.05) remained an independent predictor of CAD by logistic regression analysis. These results highlight postchallenge proinflammatory and nitrosative responses by 75 g-OGTT, rather than hyperglycemia per se, are associated with CAD in patients without previous recognized diabetes.

Tài liệu tham khảo

Kannel WB, McGee DL: Diabetes and cardiovascular diseases: the Framingham study. JAMA. 1979, 241: 2035-2038. 10.1001/jama.1979.03290450033020. Coutinho M, Gerstein HC, Wang Y, Yusuf S: The relationship between glucose and incident cardiovascular events: a metaregression analysis of published data from 20 studies of 95,783 individuals followed for 12.4 years. Diabetes Care. 1999, 22: 233-240. 10.2337/diacare.22.2.233. Ceriello A: Impaired glucose tolerance and cardiovascular disease: the possible role of post-prandial hyperglycemia. Am Heart J. 2004, 147: 803-807. 10.1016/j.ahj.2003.11.020. Ceriello A, Esposito K, Piconi L, Ihnat M, Thorpe J, Testa R, Bonfigli AR, Giugliano D: Glucose "peak" and glucose "spike": impact on endothelial function and oxidative stress. Diabetes Res Clin Pract. 2008, 82: 262-267. 10.1016/j.diabres.2008.07.015. The DECODE study group: Glucose tolerance and mortality: comparison of WHO and American Diabetes Association diagnostic criteria European Diabetes Epidemiology Group. Diabetes Epidemiology: Collaborative analysis of Diagnostic criteria in Europe. Lancet. 1999, 354: 617-621. Rodriguez BL, Lau N, Burchfiel CM, Abbott RD, Sharp DS, Yano K, Curb JD: Glucose intolerance and 23-year risk of coronary heart disease and total mortality: the Honolulu Heart Program. Diabetes Care. 1999, 22: 1262-1265. 10.2337/diacare.22.8.1262. UK Prospective Diabetes Study (UKPDS) Group: Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33). Lancet. 1998, 352: 837-853. Lebovitz HE: Effect of the postprandial state on nontraditional risk factors. Am J Cardiol. 2001, 88: 20H-25H. Heine RJ, Dekker JM: Beyond postprandial hyperglycaemia: metabolic factors associated with cardiovascular disease. Diabetologia. 2002, 45: 461-475. 10.1007/s00125-001-0726-0. Haffner SM: The importance of hyperglycemia in the nonfasting state to the development of cardiovascular disease. Endocr Rev. 1998, 19: 583-592. 10.1210/er.19.5.583. Biondi-Zoccai GG, Abbate A, Liuzzo G, Biasucci LM: Atherothrombosis, inflammation, and diabetes. J Am Coll Cardiol. 2003, 41: 1071-1077. 10.1016/S0735-1097(03)00088-3. Mathew M, Tay E, Cusi K: Elevated plasma free fatty acids increase cardiovascular risk by inducing plasma biomarkers of endothelial activaition, myeloperoxidase and PAI-1 in healthy subjects. Cardiovasc Diabetol. 2009, 9: 9. Sanchez R, Fischer P, Cuniberti L, Masnatta LD, Ramirez AJ: Vascular oxidative stress is associated with insulin resistance in hyper-reninemic nonmodulating essential hypertension. J Hypertens. 2007, 25: 2434-2440. 10.1097/HJH.0b013e3282f03597. Esposito K, Nappo F, Marfella R, Giugliano G, Giugliano F, Ciotola M, Quagliaro L, Ceriello A, Giugliano D: Inflammatory cytokine concentrations are acutely increased by hyperglycemia in humans: role of oxidative stress. Circulation. 2002, 106: 2067-2072. 10.1161/01.CIR.0000034509.14906.AE. Beckmann JS, Ye YZ, Anderson PG, Chen J, Accavitti MA, Tarpey MM, White CR: Extensive nitration of protein tyrosines in human atherosclerosis detected by immunohistochemistry. Boil Chem Hoppe Seyler. 1994, 375: 81-88. Horvath EM, Magenheim R, Kugler E, Vacz G, Szigethy A, Levardi F, Kollai M, Szabo C, Lacza Z: Nitrative stress and poly(ADP-ribose) polymerase activation in healthy and gestational diabetic pregnancies. Diabetologia. 2009, 52: 1935-1943. 10.1007/s00125-009-1435-3. Ceriello A, Mercuri F, Quagliaro L, Assaloni R, Motz E, Tonutti L, Taboga C: Detection of nitrotyrosine in the diabetic plasma: evidence of oxidative stress. Diabetologia. 2001, 44: 834-838. 10.1007/s001250100529. Shishehbor MH, Aviles RJ, Brennan ML, Fu X, Goormastic M, Pearce GL, Gokce N, Keaney JF, Penn MS, Sprecher DL, Vita JA, Hazen SL: Association of nitrotyrosine levels with cardiovascular disease and modulation by statin therapy. JAMA. 2003, 289: 1675-1680. 10.1001/jama.289.13.1675. The Expert Committee on the Diagnosis and Classification of Diabetes Mellitus: Follow-up report on the diagnosis of diabetes mellitus The Expert Committee on the Diagnosis and Classification of Diabetes Mellitus. Diabetes Care. 2003, 26: 3160-3167. Hoffmeister A, Rothenbacher D, Bazner U, Frohlich M, Brenner H, Hombach V, Koenig W: Role of novel markers of inflammation in patients with stable coronary heart disease. Am J Cardiol. 2001, 87: 262-266. 10.1016/S0002-9149(00)01355-2. Taubert G, Winkelmann BR, Schleiffer T, Marz W, Winkler R, Gok R, Klein B, Schneider S, Boehm BO: Prevalence, predictors, and consequences of unrecognized diabetes mellitus in 3266 patients scheduled for coronary angiography. Am Heart J. 2003, 145: 285-291. 10.1067/mhj.2003.134. Norhammar A, Tenerz A, Nilsson G, Hamsten A, Efendic S, Ryden L, Malmberg K: Glucose metabolism in patients with acute myocardial infarction and no previous diagnosis of diabetes mellitus: a prospective study. Lancet. 2002, 359: 2140-2144. 10.1016/S0140-6736(02)09089-X. Satoh H, Terada H, Uehara A, Katoh H, Matsunaga M, Yamazaki K, Matoh F, Hayashi H: Post-challenge hyperinsulinaemia rather than hyperglycaemia is associated with the severity of coronary artery disease in patients without a previous diagnosis of diabetes mellitus. Heart. 2005, 91: 731-736. 10.1136/hrt.2003.032326. Hosseinpanah F, Rambod M, Reza Ghaffari HR, Azizi F: Predicting isolated postchallenge hyperglycaemia: a new approach; Tehran Lipid and Glucose Study (TLGS). Diabet Med. 2006, 23: 982-989. 10.1111/j.1464-5491.2006.01939.x. Hashimoto K, Ikewaki K, Yagi H, Nagasawa H, Imamoto S, Shibata T, Mochizuki S: Glucose intolerance is common in Japanese patients with acute coronary syndrome who were not previously diagnosed with diabetes. Diabetes Care. 2005, 28: 1182-1186. 10.2337/diacare.28.5.1182. Kanauchi M, Tsujimoto N, Hashimoto T: Advanced glycation end products in nondiabetic patients with coronary artery disease. Diabetes Care. 2001, 24: 1620-1623. 10.2337/diacare.24.9.1620. Takezako T, Saku K, Zhang B, Shirai K, Arakawa K: Insulin resistance and angiographical characteristics of coronary atherosclerosis. Jpn Circ J. 1999, 63: 666-673. 10.1253/jcj.63.666. Festa A, D'Agostino R, Tracy RP, Haffner SM: C-reactive protein is more strongly related to post-glucose load glucose than to fasting glucose in non-diabetic subjects; the Insulin Resistance Atherosclerosis Study. Diabet Med. 2002, 19: 939-943. 10.1046/j.1464-5491.2002.00824.x. Johansen OE, Birkeland KI, Brustad E, Aaser E, Lindahi AK, Midha R, Ueland T, Aukrus P, Gullestad L: Undiagnosed dysglycaemia and inflammation in cardiovascular disease. Eur J Clin Invest. 2006, 36: 544-551. 10.1111/j.1365-2362.2006.01679.x. Festa A, D'Agostino R, Howard G, Mykkanen L, Tracy RP, Haffner SM: Chronic subclinical inflammation as part of the insulin resistance syndrome: the Insulin Resistance Atherosclerosis Study (IRAS). Circulation. 2000, 102: 42-47. Lu B, Yang Y, Yang Z, Feng X, Wang X, Zhang Z, Hu R: Insulin resistance in Chinese patients with type 2 diabetes is associated with C-reactive protein independent of abdominal obesity. Cardiovasc Diabetol. 2010, 9: 92-10.1186/1475-2840-9-92. Ceriello A, Quagliaro L, Piconi L, Assaloni R, Da Ros R, Maier A, Esposito K, Giugliano D: Effect of postprandial hypertriglyceridemia and hyperglycemia on circulating adhesion molecules and oxidative stress generation and the possible role of simvastatin treatment. Diabetes. 2004, 53: 701-710. 10.2337/diabetes.53.3.701. Dinh W, Futh R, Nickl W, Krahn T, Ellinghaus p, Scheffold T, Bansemir L, Bufe A, Barroso MC, Lankisch M: Elevated plasma levels of TNF-alpha and Interleukin-6 in patients with diastolic dysfunction and glucose metabolism disorders. Cardiovasc Diabetol. 2009, 8: 58-10.1186/1475-2840-8-58. Lindmark E, Diderholm E, Wallentin L, Siegbahn A: Relationship between interleukin-6 and mortality in patients with unstable coronary artery disease: effects of an early invasive or noninvasive strategy. JAMA. 2001, 286: 2107-2113. 10.1001/jama.286.17.2107. Oberbach A, Tonjes A, Kloting N, Fasshauer M, Kratzsch J, Bussee MW, Paschke R, Stumvoll M, Bluher M: Effect of a 4 week physical training program on plasma concentrations of inflammatory markers in patients with abnormal glucose tolerance. Eur J endocrinol. 2006, 154: 577-585. 10.1530/eje.1.02127.