Advances in Clinical and Experimental Medicine
2008, vol. 17, nr 5, September-October, p. 565–573
Publication type: review article
Language: English
Disorders in Postprandial Lipid Metabolism and the Risk of Atherogenesis
Nadmierna lipemia poposiłkowa jako czynnik ryzyka miażdżycy
1 Department of Internal and Occupational Medicine and Hypertension, Silesian Piasts University of Medicine in Wrocław, Poland
Abstract
Postprandial hyperlipidemia (lipemia) is a frequent metabolic disorder observed in diabetes mellitus and atherosclerosis. The postprandial state after a high−fat meal induces endothelial dysfunction, mainly through an oxidative stress mechanism. Postprandial hyperlipidemia is known to reduce endothelium−dependent flow−mediated vasodilatation (FMD). Endothelial dysfunction has been suggested to be an early indicator of atherosclerosis. Postprandial hyperlipidemia may contribute to the development of coronary artery disease (CAD) because it is frequently observed in patients with premature atherosclerosis, despite relatively normal fasting lipemia. Hyperlipidemia has also been reported to be associated with an increased expression of cellular adhesion molecules. Postprandial intravascular inflammatory changes may be an important link in the pathogenesis of atherosclerosis.
Streszczenie
Hiperlipidemia poposiłkowa jest częstym zaburzeniem metabolicznym towarzyszącym cukrzycy i miażdżycy. Dysfunkcja śródbłonka po wysokotłuszczowym posiłku jest indukowana głównie wskutek stresu oksydacyjnego. Hiperlipidemia poposiłkowa jest uważana za czynnik ograniczający zależną od śródbłonka wazodylatację indukowaną przepływem (FMD – flow mediated vasodilatation). Dysfunkcję śródbłonka uważa się za wczesny wskaźnik miażdżycy. Poposiłkowa hiperlipidemia może przyczyniać się do rozwoju choroby niedokrwiennej serca, ponieważ jest często obecna u chorych z przedwcześnie występującą miażdżycą, mimo prawidłowej lipemii na czczo. Hiperlipidemia jest także związana z nasiloną ekspresją cząsteczek adhezji komórkowej. Zmiany zapalne wewnątrz naczynia w fazie poposiłkowej mogą być istotnym ogniwem patogenetycznym miażdżycy.
Key words
atherosclerosis, postprandial lipemia, hypertriacylglycerolemia, endothelial dysfunction, inflammation
Słowa kluczowe
miażdżyca, lipemia poposiłkowa, hipertriacyloglicerolemia, dysfunkcja śródbłonka, zapalenie
References (54)
- Nitenberg A, Cosson E, Pham I: Postprandial endothelial dysfunction: role of glucose, lipids and insulin. Diabetes Metab 2006, 32, 28–33.
- Tripathy D, Mohanty P, Dhindsa S, Syed T, Ghanim H, Aljada A, Dandona P: Elevation of free fatty acids induces inflammation and impairs vascular reactivity in healthy subjects. Diabetes 2003, 52, 2882–2887.
- Maggi FM, Raselli S, Grigore L, Redaelli L, Fantappie S: Lipoprotein Remnants and Endothelial Dysfunction in the Postprandial Phase. J Clin Endocrinol Metab 2004, 89, 6, 2946–2950.
- Lundman P, Eriksson MJ, Stuhlinger M, Cooke JP, Hamsten A, Tornva P: Mild to moderate hypertriglyceridemia in young men is associated with endothelial dysfunction and increased plasma concentrations of asymmetric dimethylarginine. J Am Coll Cardiol 2001, 38, 111–116.
- Sejda T, Kovar J, Pitha J, Cifkova R, Svandova E, Poledne R: The effect of an acute fat load on endothelial function after different dietary regimens in young healthy volunteers. Physiol Res 2002, 51, 99–105.
- Westphal S, Taneva E, Kästner S, Martens−Lobenhoffer J, Bode−Böger S, Kropf S, Dierkes J, Luley C: Atherosclerosis 2006, 185, 2, 313–319.
- Giannattasio C, Zoppo A, Gentile G, Failla M, Capra A, Maggi FM, Catapano A: Acute Effect of High−Fat Meal on Endothelial Function in Moderately Dyslipidemic Subjects. Arterioscler Thromb Vasc Biol 2005, 25, 406–410.
- Elosua R, Ordovas JM, Cupples LA, Lai C−Q, Demissie S, Fox CS, Polak JF, Wolf PA, D’Agostino RB, O’Donnell CJ: Variants at the apoA5 locus, association with carotid atherosclerosis, and a modification by obesity: the Framingham Study. J Lipid Res 2006, 47, 990–996.
- Yamada Y, Kato K, Hibino T, Yokoi K, Matsuo H, Ichihara S, Yoshida H, Satoh K, Nozawa Y: Prediction of genetic risk for metabolic syndrome. Atherosclerosis 2007, 191, 298–304.
- Hsu L−A, Ko Y−L, Chang C−J, Hu C−F, Wu S, Teng M−S, Wang C−L, Ho W−J, Ko Y−S, Hsu T−S, Lee Y−S: Genetic variations of apolipoprotein a5 gene is associated with the risk of coronary artery disease among Chinese in Taiwan. Atherosclerosis 2006,185, 143–149.
- Kim JY, Kim OY, Koh SJ, Jang Y, Yun SS, Ordovas JM, Lee JH: Comparison of low−fat and high−fat meal on postprandial lipaemic response in non−obese men according to the –1131T>C polymorphism of the apolipoprotein A5 (apoA5) gene (randomized cross−over design). J Am Coll Nutr 2006, 25, 340–347.
- Qi L, Liu S, Rifai N, Hunter D, Hu FB: Associations of the apolipoprotein A1/C3/A4/A5 gene cluster with triglyceride and HDL cholesterol levels in women with type 2 diabetes. Atherosclerosis 2007, 192, 204–210.
- Wright WT, Young IS, Nicholls DP, Patterson C, Lyttle K, Graham CA: SNPs at the ApoA5 gene account for the strong association with hypertriglyceridemia at the ApoA5/A4/C3/A1 gene locus on chromosome 11q23 in the Northern Irish population. Atherosclerosis 2006, 185, 353–360.
- Van der Vleuten GM, Isaacs A, Zeng WW, van Duijn CM, Stalenhoef AF, de Graaf J: Haplotype analyses of the APOA5 gene in patients with familial combined hyperlipidemia. Biochim Biophys Acta 2007, 1772, 81–88.
- Henneman P, Schaap FG, Havekes LM, Rensen PCN, Frants RR, van Tol A, Hatori H, Smelt AHM, van Dijk KW: Plasma apo A5 levels are markedly elevated in severe hypertriglyceridemia and positively correlated with the apoA5 S19W polymorphism. Atherosclerosis 2007, 193, 129–134.
- Olano−Martin E, Abraham EC, Gill−Garrison, Valdes A: Influence of ApoA5 gene variants on postprandial triglyceride metabolism: Impact of gender. J Lipid Res 2008, 49, 945–953.
- Ridker PM, Rifai N, MJ Stampfer, Hennekens CH: Plasma concentration of interleukin−6 and the risk of future myocardial infarction among apparently healthy men. Circulation 2000, 101, 1767–1772.
- Muscari AG, Massarelli L, Bastagli G, Poggiopollini V, Tomassetti G, Drago C, Martignani P, Pacilli P, Boni, Puddu P: Relationship of serum C3 to fasting insulin, risk factors and previous ischaemic events in middle−aged men. Eur Heart J 2000, 21, 1081–1090.
- Van Oostrom AJHHM, Sijmonsma TP, Verseyden C, Jansen EHJM, de Koning EJP, Rabelink J, Castro Cabezas M: Postprandial recruitment of neutrophils may contribute to endothelial dysfunction. J Lipid Res 2003, 44, 576–583.
- Alipour A, Elte JW, van Zaanen HC, Rietveld AP, Cabezas MC: Postprandial inflammation and endothelial dysfuction Biochem Soc Trans 2007, 466–469.
- Takeshita S, Hashimoto H, Ono Y, Ochiai M, Yokoyama N, Terakura M, Sato T, Isshiki T: Increased leukocyte activity as a predictor for flow−limiting coronary lesions in patients with angina pectoris. Atherosclerosis 2001, 158, 477–481.
- Hansen K, Sickelmann F, Pietrowsky R, Fehm HL, Born J: Systemic immune changes following meal intake in humans. Am J Physiol 1997, 273, 548–553.
- Esposito K, Nappo F, Giugliano F, Giugliano G, Marfella R, Giugliano D: Effect of dietary antioxidants on postprandial endothelial dysfunction induced by a high−fat meal in healthy subjects. Am J Clin Nutr 2003, 77, 139–143.
- Loscalzo J: What we know and don’t know about L−arginine and NO. Circulation 2000,101, 2126–2129.
- Ridker PM, Hennekens CH, Roitman−Johnson B, Stampfer MJ, Allen J: Plasma concentration of soluble intercellular adhesion molecule 1 and risks of future myocardial infarction in apparently healthy men. Lancet 1998, 351, 88–92.
- Ceriello A, Falleti E, Bortolotti N, Motz E, Cavarape A, Russo A, Gonano F, Bartoli E: Increased circulating intercellular adhesion molecule−1 levels in type II diabetic patients: the possible role of metabolic control and oxidative stress. Metabolism 1996, 45, 498–501.
- Otsuki M, Hashimoto K, Morimoto Y, Kishimoto T, Kasayama S: Circulating vascular cell adhesion molecule−1 (VCAM−1) in atherosclerotic NIDDM patients. Diabetes 1997, 46, 2096–2101.
- 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.
- Ceriello A, Quagliaro L, Piconi L, Assaloni R, Da Ros R, Maier A, Esposito K: 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.
- Jagla A, Schrezenmeir J: Postprandial triglycerides and endothelial function. Exp Clin Endocrinol Diabetes 2001, 109, 533–547.
- Shishehbor MH, Aviles RJ, Brennan ML, Fu X, Goormastic M, Pearce GL, Gokce N, Keaney JF Jr, 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.
- Plotnick GD, Corretti MC, Vogel RA: Effect of antioxidant vitamins on the transient impairment of endothelium−dependent brachial artery vasoactivity following a single high−fat meal. JAMA 1997, 278, 1682–1686.
- Williams MJA, Sutherland WHF, McCormick MP et al.: Impaired endothelial function following a meal rich in used cooking fat. J Am Coll Cardiol 1999, 33, 1050–1056.
- Anderson RA, Evans ML, Ellis GR, Graham J, Morris K, Jackson SK, Lewis MJ, Rees A, Frenneaux MP: The relationship between postprandial lipaemia, endothelial function and oxidative stress in healthy individuals and patients with type 2 diabetes. Atherosclerosis 2001, 154, 475–483.
- Bae JH, Bassenge E, Kim KB, Kim YN, Kim KS, Lee HJ, Moon KC, Lee MS, Park KY, Schwemmer M: Postprandial hypertriglyceridemia impairs endothelial function by enhanced oxidant stress. Atherosclerosis 2001, 155, 517–523.
- Bae JH, Schwemmer M, Lee IK, Lee HJ, Park KR, Kim KY, Bassenge E: Postprandial hypertriglyceridemiainduced endothelial dysfunction in healthy subjects is independent of lipid oxidation. Int J Cardiol 2003, 87, 259–267.
- Ridker PM, Hennekens CH, Buring JE, Rifai N: C−reactive protein and other markers of inflammation in the prediction of cardiovascular disease in women. N Engl J Med 2000, 342, 836–843.
- Ebenbichler CF, Kirchmair R, Egger C, Patsch JR: Postprandial state and atherosclerosis. Curr Opin Lipidol 1995, 6, 286–290.
- Ferrer F, Nazih H, Zaïr Y, Krempf M, Bard JM: Postprandial changes in the distribution of apolipoprotein AIV between apolipoprotein band non apolipoprotein b-containing lipoproteins in obese women. Metabolism 2003, 52, 12, 1537–1541.
- Shimabukuro M, Chinen I, Higa N, Takasu N, Yamakawa K, Ueda S: Effects of dietary composition on postprandial endothelial function and adiponectin concentrations in healthy humans: a crossover controlled study. Am J Clin Nutr 2007, 86, 4, 923–928.
- Vershuren WMM, Jacobs DR, Bloemberg BPM, et al. Serum total cholesterol and long−term coronary heart disease mortality in different cultures. JAMA 1995, 274, 131–136.
- Weintraub MS, Grosskopf I, Rassin T, Miller H, Charach G, Rotmensch HH, Liron M, Rubinstein A, Iaina A: Clearance of chylomicron remnants in normolipidaemic patients with coronary artery disease: case control study over three years. BMJ 1996, 312, 936–939.
- Ceriello A: The possible role of postprandial hyperglycaemia in the pathogenesis of diabetic complications. Diabetologia 2003, 46, 9–16.
- Bae JH, Bassenge E, Kim KB, Kim YN, Kim KS, Lee HJ, Moon KC, Lee MS, Park KY, Schwemmer M: Postprandial hypertriglyceridemia impairs endothelial function by enhanced oxidant stress. Atherosclerosis 2001, 155, 517–523.
- Simpson HS, Williamson CM, Olivecrona T, Pringle S, Maclean J, Lorimer AR, Bonn Bogaievsky Y, Packard CJ, Shepherd J: Postprandial lipemia, fenofibrate and coronary artery disease. Atherosclerosis 1990, 85, 193–202.
- Austin MA, Kokanson JE, Edwards KL: Hypertriglyceridemia as a cardiovascular risk factor. Am J Cardiol 1998, 81, 7–12.
- Chowienczyk PJ, Watts GF, Wierzbicki AS, Cockcroft JR, Brett SE, Ritter JM: Preserved endothelial function in patients with severe hypertriglyceridemia and low functional lipoprotein lipase activity. J Am Coll Cardiol 1997, 29, 964–968.
- Matsumoto K, Sera Y, Ueki Y, Inukai G, Niiro E, Miyake S: Comparison of serum concentrations of soluble adhesion molecules in diabetic microangiopathy and macroangiopathy. Diabet Med 2002, 19, 822–826.
- Rizzoni D, Muiesan ML, Porteri E, Castellano M, Salvetti M, Montero C, De Ciuccis C, Boari G, Valentini U, Cimino A, Sleiman I, Agabiti E: Circulating adhesion molecules and carotid artery structural changes in patients with noninsulin−dependent diabetes mellitus. J Hum Hypertens 2004, 17, 463–470.
- Bell DS, O'Keefe JH, Jellinger P: Postprandial dysmetabolism: the missing link between diabetes and cardiovascular events? Endocr Pract 2008, 14, 1, 112–124.
- Cortés B, Núñez I, Cofán M, Gilabert R, Pérez−Heras A, Casals E, Deulofeu R, Ros E: Acute effects of highfat meals enriched with walnuts or olive oil on postprandial endothelial function. J Am Coll Cardiol 2006, 17, 48, 8, 1666–1671.
- Ceriello A, Assaloni R, Da Ros R, Maier A, Piconi L, Quagliaro L: Effect of Atorvastatin and Irbesartan, Alone and in Combination, on Postprandial Endothelial Dysfunction, Oxidative Stress, and Inflammation in Type 2 Diabetic Patients. Circulation 2005, 111, 2518–2524.
- Christ M, Bauersachs J, Liebetrau C, Heck M, Gunther A, Wehling M: Glucose increases endothelial−dependent superoxide formation in coronary arteries by NAD(P)H oxidase activation: attenuation by the 3−hydroxy−3− −methylglutaryl coenzyme A reductase inhibitor atorvastatin. Diabetes 2002, 51, 2648–2652.
- Rueckschloss U, Quinn MT, Holtz J, Morawietz H: Dose−dependent regulation of NAD(P)H oxidase expression by angiotensin II in human endothelial cells: protective effect of angiotensin II type 1 receptor blockade in patients with coronary artery disease. Arterioscler Thromb Vasc Biol 2002, 22, 1845–1851.