Información del artículo
Se ha asociado la hiperlipemia posprandial a componentes del síndrome metabólico y mayor riesgo de enfermedad cardiovascular. Se define como una elevación de las concentraciones plasmáticas de triglicéridos tras la ingestión de grasa.
Se ha descrito la relación del síndrome metabólico con el estrés oxidativo. Por un lado, en sujetos obesos se observa un incremento de la producción de especies reactivas de oxígeno que deteriora la secreción de insulina y conduce a un aumento de la producción de adipocinas. Y por otro lado, se ha visto que el papel antioxidante de las concentraciones plasmáticas de lipoproteínas de alta densidad está mermado en circunstancias de hipertrigliceridemia, hiperinsulinemia y resistencia a la insulina.
Este incremento del estrés oxidativo y la producción de citocinas es más patente durante el estado posprandial. También se observa un aumento de las moléculas de adhesión celular, y todo esto lleva a daño vascular y disfunción endotelial.
En todo este maremágnum de sucesos, ¿qué papel tiene la hiperuricemia? ¿Las cifras elevadas de ácido úrico son un marcador de riesgo cardiovascular o un factor de riesgo cardiovascular? Por un lado está la producción de radicales superóxidos, por otro lado está el efecto antioxidante del propio ácido úrico. Esta paradoja ha motivado que aparezcan trabajos donde se demuestra que la administración de alopurinol, que es hipouricemiante, reduce las especies reactivas de oxígeno, y otros donde se observa que la elevación de las cifras de ácido úrico incrementa la capacidad antioxidante del plasma.
Palabras clave:
Hiperlipemia posprandial
Estrés oxidativo
Síndrome metabólico
Ácido úrico
Hiperuricemia
Postprandial hyperlipidemia has been associated with components of the metabolic syndrome and an increased risk of cardiovascular disease. It is defined as an elevation of plasma triglyceride levels after fat intake.
An association between the metabolic syndrome and oxidative stress has been described. On the one hand, obese subjects showed increased production of reactive oxygen species, reducing insulin secretion and leading to increased adipokine production. On the other hand, the antioxidant role of plasma high-density lipoprotein levels is reduced in situations of hypertriglyceridemia, hyperinsulinemia and insulin resistance.
This increase of oxidative stress and cytokine production is more evident during postprandial states. Moreover, an increase in cell adhesion molecules has also been observed, all of which leads to vascular injury and endothelial dysfunction.
What is the role of hyperuricemia among all these events? Are elevated uric acid levels a marker for cardiovascular risk or a cardiovascular risk factor? On the one hand, there is superoxide radical production and on the other, the antioxidant effect of uric acid. This paradox has led to the publication of some studies that demonstrate that allopurinol administration, which lowers uric acid levels, reduces reactive oxygen species and to others that show that elevation of uric acid levels increases the antioxidant ability of plasma
Key words:
Postprandial hyperlipidemia
Oxidative stress
Metabolic syndrome
Uric acid
Hyperuricemia
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Bibliografía
[1.]
C. Couillard, N. Bergeron, J.A. Bergeron, A. Pascot, P. Mauriege, A. Tremblay, et al.
Metabolic heterogeneity underlying postprandial lipemia among men with low fasting high density lipoprotein cholesterol concentrations.
J Clin Endocrinol Metab, 85 (2000), pp. 4575-4582
[2.]
G.D. Kolovou, K.K. Anagnostopoulou, A.N. Pavlidis, K.D. Salpea, S.A. Iraklianou, K. Tsarpalis, et al.
Postprandial lipemia in men with metabolic syndrome, hypertensives and healthy subjects.
Lipids Health Dis, 4 (2005), pp. 21
[3.]
F. Karpe.
Postprandial lipoprotein metabolism and atherosclerosis.
J Intern Med, 246 (1999), pp. 341-355
[4.]
M.E. Tushuizen, M. Diamant, R.J. Heine.
Postprandial dysmetabolism and cardiovascular disease in type 2 diabetes.
Postgrad Med J, 81 (2005), pp. 1-6
[5.]
A. Tanaka.
Postprandial hyperlipidemia and atherosclerosis.
J Atheroscler Thromb, 11 (2004), pp. 322-329
[6.]
M. Castro-Cabezas.
Postprandial lipaemia in familial combined hyperlipidaemia.
Biochem Soc Trans, 31 (2003), pp. 1090-1093
[7.]
F. Cardona, S. Morcillo, M. Gonzalo-Marin, F.J. Tinahones.
The apolipoprotein E genotype predicts postprandial hypertriglyceridemia in patients with the metabolic syndrome.
J Clin Endocrinol Metab, 90 (2005), pp. 2972-2975
[8.]
D.S. Pettit, K.J. Cureton.
Effects of prior exercise on postprandial lipemia. A quantitative review.
Metabolism, 52 (2003), pp. 418-424
[9.]
K.G. Jackson, J.M. Knapper-Francis, L.M. Morgan, D.H. Webb, A. Zampelas, C.M. Williams.
Exaggerated postprandial lipaemia and lower post-heparin lipoprotein lipase activity in middle-aged men.
Clin Sci (Lond), 105 (2003), pp. 457-466
[10.]
A.P. Van Beeck, F.C. Ruijter-Hejstek, D.W. Erkelens, T.W. de Bruin.
Menopause is associated with reduced protection from postprandial lipemia.
Arterioscler Thromb Vasc Biol, 19 (1999), pp. 2737-2741
[11.]
M.J. Albrink, E.B. Man.
Serum triglycerides in coronary artery disease.
AMA Arch Intern Med, 103 (1959), pp. 4-8
[12.]
F. Karpe, G. Steiner, K. Uffelman, T. Olivecrona, A. Hamsten.
Postprandial lipoproteins and progression of coronary atherosclerosis.
Atherosclerosis, 106 (1994), pp. 83-97
[13.]
B. Isomaa, P. Almgren, T. Tuomi, B. Forsen, K. Lahti, M. Nissen, et al.
Cardiovascular morbidity and mortality associated with the metabolic syndrome.
Diabetes Care, 24 (2001), pp. 683-689
[14.]
E.S. Ford, W.H. Giles, W.H. Dietz.
Prevalence of the metabolic syndrome among US adults: findings from the Third National Health and Nutrition Examination Survey.
JAMA, 287 (2002), pp. 356-359
[15.]
Grundy SM, Brewer HB Jr, Cleeman JI, Smith SC Jr, Lenfant C, National Heart Lung and Blood Institute, American Heart Association, et al. Definition of metabolic syndrome: Report of the National Heart, Lung, and Blood Institute/American Heart Association conference on scientific issues related to definition. Circulation. 2004;109:433-8.
[16.]
I. Shimomura, T. Funahashi, M. Takahashi, K. Maeda, K. Kotani, T. Nakamure, et al.
Enhanced expression of PAI-1 in visceral fat: possible contributor to vascular disease in obesity.
Nat Med, 2 (1996), pp. 800-803
[17.]
G.S. Hotamisligil, N.S. Shargill, B.M. Spiegelman.
Adipose expression of tumor necrosis factor-α: direct role in obesity-linked insulin resistance.
Science, 259 (1993), pp. 87-91
[18.]
K.T. Uysal, S.M. Wiesbrock, M.W. Marino, G.S. Hotamisligil.
Protection from obesity-induced insulin resistance in mice lacking TNF-alpha function.
Nature, 389 (1997), pp. 610-614
[19.]
S.K. Fried, D.A. Bunkin, A.S. Greenberg.
Omental and subcutaneous adipose tissues of obese subjects release interleukin-6: depot difference and regulation by glucocorticoid.
J Clin Endocrinol Metab, 83 (1998), pp. 847-850
[20.]
P. Sartipy, D.J. Loskutoff.
Monocyte chemoattractant protein 1 in obesity and insulin resistance.
Proc Natl Acad Sci USA, 100 (2003), pp. 7265-7270
[21.]
I. Hainault, G. Nebout, S. Turban, B. Ardouin, P. Ferre, A. Quignard-Boulangé.
Adipose tissue-specific increase in angiotensinogen expression and secretion in the obese (fa/fa) zucker rat.
Am J Physiol Endocrinol Metab, 282 (2002), pp. E59-E66
[22.]
A.H. Berg, T.P. Combs, P.E. Scherer.
ACRP30/adiponectin: An adipokine regulating glucose and lipid metabolism.
Trends Endocrinol Metab, 13 (2002), pp. 84-89
[23.]
T.S. Tsao, H.F. Lodish, J. Fruebis.
ACRP30, a new hormone controlling fat and glucose metabolism.
Eur J Pharmacol, 440 (2002), pp. 213-221
[24.]
Y. Matsuzawa, T. Funahashi, S. Kihara, J. Shimomura.
Adiponectin and metabolic syndrome.
Arterioscler Thromb Vasc Biol, 24 (2004), pp. 29-33
[25.]
J.M. Friedman, J.L. Halaas.
Leptin and the regulation of body weight in mammals.
Nature, 395 (1998), pp. 763-770
[26.]
I.S. Farooqi, J.M. Keogh, S. Kamath, S. Jones, W.T. Gibson, R. Trusell, et al.
Partial leptin deficiency and human adiposity.
Nature, 414 (2001), pp. 34-35
[27.]
R.H. Unger.
The physiology of cellular liporegulation.
Annu Rev Physiol, 65 (2003), pp. 333-347
[28.]
S. Furukawa, T. Fujita, M. Shimabukuro, H. Iwaki, Y. Yamada, Y. Nakajima, et al.
Increased oxidative stress in obesity and its impact on metabolic syndrome.
J Clin Invest, 114 (2004), pp. 1752-1761
[29.]
T. Yamauchi, J. Kamon, H. Waki, Y. Terauchi, N. Kubota, K. Hara, et al.
The fat-derived hormone adiponectin reverses insulin resistance associated with both lipoatrophy and obesity.
Nat Med, 7 (2001), pp. 941-946
[30.]
M. Bajaj, S. Suraamornkul, P. Piper, L.J. Hardies, L. Glass, E. Cersosimo, et al.
Decreased plasma adiponectin concentrations are closely related to hepatic fat content and hepatic insulin resistance in pioglitazone treated type 2 diabetic patients.
J Clin Endocrinol Metab, 89 (2004), pp. 200-206
[31.]
C. Weyer, T. Funahashi, S. Tanaka, K. Hotta, Y. Matsuzawa, R.E. Pratley, et al.
Hypoadiponectinemia in obesity and type 2 diabetes. close association with insulin resistance and hyperinsulinemia.
J Clin Endocrinol Metab, 86 (2001), pp. 1930-1935
[32.]
C.S. Mantzoros, T. Li, J.E. Manson, J.B. Meigs, F.B. Hu.
Circulating adiponectin levels are associated with better glycemic control, more favorable lipid profile, and reduced inflammation in women with type 2 diabetes.
J Clin Endocrinol Metab, 90 (2005), pp. 4542-4548
[33.]
K. Nakazono, N. Watanabe, K. Matsuno, J. Sasaki, T. Sato, M. Inoue.
Does superoxide underlie the pathogenesis of hypertension?.
Proc Natl Acad Sci USA, 88 (1991), pp. 10045-10048
[34.]
Y. Ohara, T.E. Peterson, D.G. Harrison.
Hypercholesterolemia increases endothelial superoxide anion production.
J Clin Invest, 91 (1993), pp. 2546-2551
[35.]
T. Roskams, T. Roskams, S.Q. Yang, A. Koteish, A. Durnez, R. De-Vos, et al.
Oxidative stress and oval cell accumulation in mice and humans with alcoholic and nonalcoholic fatty liver disease.
Am J Pathol, 163 (2003), pp. 1301-1311
[36.]
B. Hansel, P. Giral, E. Nobecourt, S. Chantepie, E. Bruckert, M.J. Chapman, et al.
Metabolic syndrome is associated with elevated oxidative stress and dysfunctional dense high-density lipoprotein particles displaying impaired antioxidative activity.
J Clin Endocrinol Metab, 89 (2004), pp. 4963-4971
[37.]
W. Patsch, H. Esterbauer, B. Foger, J.R. Patsch.
Postprandial lipemia and coronary risk.
Curr Atheroscler Rep, 2 (2000), pp. 232-242
[38.]
Cardona F, Morcillo S, Garrido-Sanchez L, et al. Pro12Ala polymorphism of the PPAR gamma gene is associated with postprandial hypertriglyceridaemia in non E3/E3 patients with the metabolic syndrome. Am J Clin Nutr. [en prensa].
[39.]
Cardona F, Tinahones FJ. Relación de la hipertrigliceridemia postprandial con la resistencia a la insulina en pacientes con síndrome metabólico. Endocrinol. [en prensa].
[40.]
Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults.
Executive Summary of The Third Report of The National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, And Treatment of High Blood Cholesterol In Adults (Adult Treatment Panel III).
JAMA, 285 (2001), pp. 2486-2497
[41.]
J.F. Tinahones, G. Pérez-Lindon, F.J. C-Soriguer, A. Pareja, P. Sanchez-Guijo, E. Collantes.
Dietary alterations in plasma very low density lipoprotein levels modify renal excretion of urates in hyperuricemic-hypertriglyceridemic patients.
J Clin Endocrinol Metab, 82 (1997), pp. 1188-1191
[42.]
F. Cardona, F.J. Tinahones, E. Collantes, A. Escudero, E. Garcia-Fuentes, F.J. Soriguer.
The elevated prevalence of apolipoprotein E2 in patients with gout is associated with reduced renal excretion of urates.
Rheumatology (Oxford), 42 (2003), pp. 468-472
[43.]
F. Cardona, F.J. Tinahones, E. Collantes, A. Escudero, E. Garcia-Fuentes, F.J. Soriguer.
Contribution of polymorphisms in the apolipoprotein AI- CIII-AIV cluster to hyperlipidaemia in patients with gout.
Ann Rheum Dis, 64 (2005), pp. 85-88
[44.]
D.B. Zilversmit.
A proposal linking atherogenesis to the interaction of endothelial lipoprotein lipase with triglyceride-rich lipoproteins.
Circ Res, 33 (1973), pp. 633-638
[45.]
D.B. Zilversmit.
Atherogenic nature of triglycerides, postprandial lipidemia, and triglyceride-rich remnant lipoproteins.
Clin Chem, 41 (1995), pp. 153-158
[46.]
K. Kusterer, T. Pohl, H.P. Fortmeyer, W. Marz, H. Scharnagl, A. Oldenburg, et al.
Chronic selective hypertriglyceridemia impairs endotheliumdependent vasodilatation in rats.
Cardiovasc Res J, 42 (1999), pp. 783-793
[47.]
E.J. De Koning, T.J. Rabelink.
Endothelial function in the postprandial state.
Atheroscler Suppl, 3 (2002), pp. 11-16
[48.]
J.M. Gill, M.J. Caslake, C. McAllister, F. Tsofliu, W.R. Ferrell, C.J. Packard, et al.
Effects of short-term detraining on postprandial metabolism, endothelial function, and inflammation in endurance-trained men: dissociation between changes in triglyceride metabolism and endothelial function.
J Clin Endocrinol Metab, 88 (2003), pp. 4328-4335
[49.]
W.Q. Gradek, M.T. Harris, N. Yahia, W.W. Davis, N.A. Le, W.V. Brown.
Polyunsaturated fatty acids acutely suppress antibodies to malondialdehyde-modified lipoproteins in patients with vascular disease.
Am J Cardiol, 93 (2004), pp. 881-885
[50.]
P.E. Bowen, G. Borthakur.
Postprandial lipid oxidation and cardiovascular disease risk.
Curr Atheroscler Rep, 6 (2004), pp. 477-484
[51.]
A. Ceriello, L. Quagliaro, L. Piconi, R. Assaloni, R. Da Ros, A. Maier, et al.
Effect of postprandial hypertriglyceridemia and hyperglycemia on circulating adhesion molecules and oxidative stress generation and the possible role of simvastatin treatment.
Diabetes, 53 (2004), pp. 701-710
[52.]
A. Moers, S. Fenselau, J. Schrezenmeir.
Chylomicrons induce E-selectin and VCAM-1 expression in endothelial cells.
Exp Clin Endocrinol Diab, 105 (1997), pp. 35-37
[53.]
P. Lundman, P. Tornvall, L. Nilsson, J. Pernow.
A triglyceriderich fat emulsion and free fatty acids but not very low densitiy lipoproteins impair endotheliumdependent vasorelaxation.
Atherosclerosis, 159 (2001), pp. 35-41
[54.]
F. Nappo, K. Esposito, M. Cioffi, G. Giuliano, A.M. Molinari, G. Paolisso, et al.
Postprandial endothelial function in healthy subjects and in type 2 diabetic patients: role of fat and carbohydrate meals.
J Am Coll Cardiol, 39 (2002), pp. 1145-1150
[55.]
J.H. Bae, E. Bassenge, K.B. Kim, Y.N. Kim, K.S. Kim, H.J. Lee, et al.
Postprandial hypertriglyceridemia impairs endothelial function by enhanced oxidant stress.
Atherosclerosis, 155 (2001), pp. 517-523
[56.]
R.A. Anderson, M.L. Evans, G.R. Ellis, J. Graham, K. Morris, S.K. Jackson, et al.
The relationships between post-prandial lipaemia, endothelial function and oxidative stress in healthy individuals and patients with type 2 diabetes.
Atherosclerosis, 154 (2001), pp. 475-483
[57.]
R. Saxena, S.V. Madhu, R. Shukla, K.M. Prabhu, J.K. Gambhir.
Postprandial hypertriglyceridemia and oxidative stress in patients of type 2 diabetes mellitus with macrovascular complications.
Clin Chim Acta, 359 (2005), pp. 101-108
[58.]
G.F. Watts, D.A. Playford.
Dyslipoproteinaemia and hyperoxidative stress in the pathogenesis of endothelial dysfunction in non-insulin dependent diabetes mellitus: an hypothesis.
Atherosclerosis, 141 (1998), pp. 17-30
[59.]
A. Ceriello, R. Assaloni, R. Da Ros, A. Maier, L. Piconi, L. Quagliaro, et al.
Effect of atorvastatin and irbesartan, alone and in combination, on postprandial endothelial dysfunction, oxidative stress, and inflammation in type 2 diabetic patients.
Circulation, 111 (2005), pp. 2518-2524
[60.]
G. Arcaro, A. Cretti, S. Balzano, A. Lechi, M. Muggeo, E. Bonora, et al.
Insulin causes endothelial dysfunction in humans: sites and mechanisms.
Circulation, 105 (2002), pp. 576-582
[61.]
Kylin E: Studien ueber das Hypertonie-Hyperglyka “mie-Hyperurika” miesyndrom. Zentralblatt fuer Innere Medizin. 1923, 44:105-27.
[62.]
G.M. Reaven.
Banting lecture 1988. Role of insulin resistance in human disease.
Diabetes, 37 (1988), pp. 1595-1607
[63.]
I. Zavaroni, S. Mazza, M. Fantuzzi, E. Dall’Aglio, E. Bonora, R. Delsignore, et al.
Changes in insulin and lipid metabolism in males with asymptomatic hyperuricaemia.
J Intern Med, 234 (1993), pp. 25-30
[64.]
F.J. Tinahones, E. Collantes, F.J. C-Soriguer, A. Gonzalez-Ruiz, M. Pineda, J. Anon, et al.
Increased VLDL levels and disminished renal excretion of uric acid in hyperuricemic-hypertrigliceridemic patients.
Br J Rheumatol, 34 (1995), pp. 920-924
[65.]
C.E. Berry, J.M. Hare.
Xanthine oxidoreductase and cardiovascular disease: molecular mechanisms and pathophysiological implications.
J Physiol, 16 (2004), pp. 589-606
[66.]
C.A. Farquharson, R. Butler, A. Hill, J.J. Belch, A.D. Struthers.
Allopurinol improves endotelial dysfunction in chronic heart failure.
Circulation, 106 (2002), pp. 221-226
[67.]
W.S. Waring, D.J. Webb, S.R. Maxwell.
Systemic uric acid administration increases serum antioxidant capacity in healthy volunteers.
J Cardiovasc Pharmacol, 38 (2001), pp. 365-371
[68.]
W.S. Waring, A. Convery, V. Mishra, A. Shenkin, D.J. Webb, S.R. Maxwell.
Uric acid reduces exercise-induced oxidative stress in healthy adults.
Clin Sci (Lond), 105 (2003), pp. 425-430
[69.]
I.F. Benzie, W. Chung, B. Tomlinson.
Simultaneous measurement of allantoin and urate in plasma: analytical evaluation and potential clinical application in oxidant:antioxidant balance studies.
Clin Chem, 45 (1999), pp. 901-904
[70.]
F. Ozguner, A. Armagan, A. Koyu, S. Caliskan, H. Koylu.
A novel antioxidant agent caffeic acid phenethyl ester prevents shock wave-induced renal tubular oxidative stress.
Urol Res, 33 (2005), pp. 239-243
[71.]
O. Elmas, M. Aslan, S. Caglar, N. Derin, A. Agar, Y. Aliciguzel, et al.
The prooxidant effect of sodium metabisulfite in rat liver and kidney.
Regul Toxicol Pharmacol, 42 (2005), pp. 77-82
[72.]
G.M. Reaven.
The metabolic syndrome: requiescat in pace.
Clin Chem, 51 (2005), pp. 931-938
[73.]
L. Parker, D.W. Lamont, N. Unwin, M.S. Pearce, S.M. Bennett, H.O. Dickinson, et al.
A lifecourse study of risk for hyperinsulinaemia, dyslipidaemia and obesity (the central metabolic syndrome) at age 49-51 years.
Diabet Med, 20 (2003), pp. 406-415
[74.]
M. Solati, A. Ghanbarian, M. Rahmani, N. Sarbazi, S. Allahverdian, F. Azizi.
Cardiovascular risk factors in males with hypertriglycemic waist (Tehran Lipid and Glucose Study).
Int J Obes Relat Metab Disord, 28 (2004), pp. 706-709
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