LOS TRIGLICÉRIDOS Y LA ATEROGÉNESIS.
Palabras clave:
Triglicéridos, aterosclerosis, lipoproteínas ricas en triglicéridos, dislipidemia, apo C-III.Resumen
Las lipoproteínas ricas en triglicéridos (TRL) comprenden los quilomicrones, las VLDL y sus remanentes. Las TRL son altamente heterogéneas, difiriendo en el tamaño, densidad, composición y riesgo cardiovascular asociado. La evidencia acumulada demuestra una fuerte correlación entre el riesgo de enfermedad cardiovascular (ECV) y el nivel de TAG en ayunas y no en ayunas (posprandial). Se han propuesto dos mecanismos por los cuales las TRL pueden incrementar la ateroesclerosis: los remanentes de TRL y las VLDL son capaces de penetrar la íntima arterial, pueden ser internalizados por los macrófagos y convertirlos en células espumosas. Segundo: durante la lipólisis de las TRL se liberan un número de lípidos inflamatorios que alteran la biología del endotelio. Los TAG no son directamente aterogénicos, pero representan un importante biomarcador de ECV a causa de su asociación con una alta concentración de partículas pequeñas y densas de LDL, niveles reducidos de colesterol HDL y con apo C-III, una proteína proinflamatoria y proaterogénica.
Referencias
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5. Cohen, D. & Fisher, E. (2013). Lipoprotein metabolism, dyslipidemia and nonalcoholic fatty liver disease. Sem Liver Dis, 33(4), 380-388.
6. Díaz, J. & Liem, A. (2005). Utilidad de la medición de la apolipoproteína B en la práctica clínica. Clin Invest Arterioscl, 7(3), 142-146.
7. Chapman, M., Ginsberg, H., Amarenco, P., Andreotti, F., Borén, J., Catapano, A., et al. (2011). Triglyceride-rich lipoproteins and high-density lipoprotein cholesterol in patients at high risk of cardiovascular disease: evidence and guiadance for management. European Heart J, 32, 1345-1361.
8. Choi, S. & Ginsberg, H. (2011). Increased Very Low Density Lipoprotein secretion, hepatic steatosis, and insulin resistance. Trends Endocrinol Metab, 22(9), 353-363.
9. Klop, B., Willem, J. & Castro-Cabezas, M. (2013). Dyslipidemia in obesity: mechanisms and potential targets. Nutrients, 5, 1218-1240.
10. Welty, F. (2013). How do elevated triglycerides and low HDL-cholesterol affect inflammation and atherothrombosis? Curr Cardiol Rep, 15(9), 378-400.
11. Vergés, B. (2015). Pathophysiology of diabetic dyslipidaemia: where are we? Diabetología, 58, 886-899.
12. Daniels, T., Killinger, K., Michal, J., Wright, R. & Jiang, Z. (2009). Lipoproteins, cholesterol homeostasis and cardiac health. Int J Biol Sciences, 5(5), 474-488.
13. Nakajima, K., Nakano, T., Tokita, Y., Nagamine, T., Inazu, A., Kobayashi, J., et al. (2011). Postprandial lipoprotein metabolism; VLDL vs chylomicrons. Clin Chem Acta, 412(15-16), 1306-1318.
14. Enkhmaa, B., Ozturk, Z., Anuurad, E. & Berglund, L. (2010). Postprandial lipoproteins and cardiovascular disease risk in diabetes mellitus. Curr Diab Rep, 10, 61-69.
15. Carey, V., Bishop, L., Laranjo, N., Harshfield, B., Kwiat, C. & Sacks, F. (2010). Controbution of high plasma triglycerides and low High-Density Lipoprotein cholesterol to residual risk of coronary heart disease after establishment of Low-Density Lipoprotein cholesterol control. Am J Cardiol, 106(6), 757-763.
16. Wan, K., Zhao, J., Huang, H., Zhang, Q., Chen, X., Zeng, Z., et al. (2015). The association between Triglyceride/High Density Lipoprotein cholesterol ratio and all-cause mortality in acute coronary syndrome after coronary revascularization. PLoS ONE, 10(4), 1-11.
17. Talayero, B. & Sacks, F. (2011). The role of triglycerides in atherosclerosis. Curr Cardiol Rep, 13(6), 544-552.
18. Bitzur, R., Cohen, H., Kamari, Y., Shaish, A. & Harats, D. (2009). Triglycerides an HDL cholesterol. Diabetes Care, 32, Supplement 2, S373-S377.
19. Kannel, W. & Vasan, R. (2009). Triglycerides as vascular risk factors: new epidemiologic insights for current opinion in cardiology. Curr Opin Cardiol, 24(4), 345-350.
20. Luo, M. & Peng, D. (2016). The emerging role of apolipoprotein C-III: beyond effects on triglyceride metabolism. Lipids in Health and Disease, 15, 1-7.
21. Han, S. H., Nicholls, S., Sakuma, I., Zhao, D. & Koh, K. K. (2016). Hipertriglyceridemia and cardiovascular diseases: revisited. Korean Circulation J, 46(2), 135-144.
22. katsanos, C. (2014). Clinical considerations and mechanistic Determinants of posprandial lipemia in older adults. Adv Nutrition, 5, 226-234.
23. Dallinga-Thie, G., Kroon, J., Borén, J. & Chapman, M. (2016). Triglyceride-rich lipoproteins and remnants: targets for therapy. Curr Cardiol Rep, 18, 1-9.
24. Golberg, I., Eckel, R. & McPherson, R. (2011). Triglycerides and heart disease, still a hypothesis? Arterioscler Thromb Vasc Biol, 31(8), 1716-1725.
25. Boren, J., Matikainen, N., Adiels, M. & Taskinen, M. R. (2014). Postprandial hypertriglyceridemia as a coronary risk factor. Clin Chim Acta, 431, 31–42.
26. Rapp, J. H., Lespine, A., Hamilton, R. L., Colyvas, N., Chaumeton, A. H., Tweedie-Hardman, J., et al. (1994). Triglyceriderich lipoproteins isolated by selected-affinity anti-apolipoprotein B immunosorption from human atherosclerotic plaque. Arterioscler Thromb Vasc Biol, 14, 1767–1774.
27. Daugherty, A., Lange, L. G., Sobel, B. E. & Schonfeld, G (1985). Aortic accumulation and plasma clearance of b-VLDL and HDL: effects of diet-induced hypercholesterolemia in rabbits. J Lipid Res, 26, 955–963.
28. Proctor, S. D. & Mamo, J. C. L. (1998). Retention of fluorescent-labelled chylomicron remnants within the intima of the arterial wall—evidence that plaque cholesterol may be derived from post-prandial lipoproteins. Eur J Clin Invest, 28, 497–504.
29. Wang, L., Gill, R., Pedersen, T., Higgins, L., Newman, J. & Rutledge, J. C. (2009). Triglyceride-rich lipprotein lipolysis releases neutral and oxidized FFAs that induce endothelial cell inflammation. J Lipid Research, 50, 204-213.
30. den Hartigh, L., Altman, R., Norman, J. & Rutledge, J. C. (2013). Posprandial VLDL lipolysis products increase monocyte adhesion and lipid droplet formation via activation of ERK2 and NFkB. Am J Physiol Heart Circ Physiol, 306, H109-H120.
31. Qamar, A., Khetarpal, S., Khera, A., Qasim, A., Rader, D. & Reilly, M. (2015). Plasma Apo C-III levels, triglycerides, and coronary artery calcification in type 2 diabetics. Arterioscler Thromb Vasc Biol, 35(8), 1880-1888.
32. Sacks, F. (2015). The crucial roles of Apolipoproteins E and C-III in ApoB lipoprotein metabolism in normolipidemia and hypertriglyceridemia. Curr Opin Lipidol, 26(1), 56-63.
33. Zheng, C., Khoo, C., Furtado, J. & Sacks, F. (2010). Apolipoprotein Hypertriglyceridemia and the dense Low-Density Lipoprotein phenotype. Circulation, 121(5), 1722-1734.
34. Gordts, P., Nock, R., Son, N. H., Ramms, B., Lew, I., Gonzales, J., et al. (2016). ApoC-III inhibits clearance of triglyceride-rich lipoproteins through LDL family receptors. J Clin Invest, 126(8), 2855-2866.
35. Tran-Dinh, A., Diallo, D., Delbosc, S., Varela-Pérez, M., Dang, Q. B., Lapergue, B., et al. (2013). HDL and endothelial Protection. British J Pharmacology, 169, 493-511.
36. Norata, G. & Catapano, A. (2005). Molecular mechanisms responsible for the antiinflammatory and protective effect of HDL on the endothelium. Vasc Health and Risk Management, 1(2), 119-129.
37. Yuhanna, I. S., Zhu, B. E., Cox, L., Hahner, S., Osborne-Lawrence, P., Lu, Y. L., et al. (2001). High-density lipoprotein binding to scavenger receptor-BI activates endothelial nitric oxide synthase. Nat Med, 7, 853-857.
38. Athyros, V., Tziomalos, K., Karangiannis, A. & Mikhailidis, D. (2011). Dyslipidaemia of obesity, metabolic syndrome and type 2 diabetes mellitus: the case for residual risk reduction after statin treatment. Open Cardiovasc Med J, 5, 24-34.
39. Shinkai, H. (2012). Cholesterol ester transfer-protein modulator and inhibitors and their potential for the treatment of cardiovascular diseases. Vascular health and risk management, 8, 323-331.
40. Jung, U. J. & Choi, M. S. (2014). Obesity and its metabolic complications: the role of adipokines and the relationship between obesity, nonalcoholic fatty liver disease. Int J Mol Sci, 15, 6184-6223.
41. Magkos, F., Mohammed, S. & Mittendorfer, B. (2008). Effect of obesity on the plasma lipoprotein subclass profile in normoglycemic and normolipidemic men and women. Int J Obes (Lond), 32(11), 1655-1664.
42. Liu, M., Chung, S., Shelness, G. & Parks, J. (2012). Hepatic ABCA1 and VLDL triglyceride production. Biochim Biophys Acta, 1821(5), 770-777.
43. Carmena, R., Duriez, P. & Fruchart, J. (2004). Atherogenic lipoprotein particles in atherosclerosis. Circulation, 15, III-2 – III-7.
44. Nikolic, D., Katsiki, N., Montalto, G., Isenovic, E., Mikhailidis, D. & Rizzo, M. (2013). Lipoprotein subfraction in metabolic syndrome and obesity: clinical significance and therapeutic approaches. Nutrients, 5, 928-948.
2. Millán, J., Pintó, X., Muñoz, A., Zúñiga, M., Rubiés-Prat, J., Pallardo, L., et al. (2009). Lipoprotein ratios: physiological significance and clinical usefulness in cardiovascular Prevention. Vasc Health Risk Prevent, 5, 757-765.
3. Toth, P. (2016). Triglyceride-rich lipoproteins as a causal factor for cardiovascular disease. Vascular Health and Risk Management, 12, 171-183.
4. Mascarenhas-Melo, F., Palabra, F., Marado, D., Sereno, J., Texeira-Lemos, E., Freitas, I., et al. (2013). Emergent biomarkers of residual cardiovascular risk in patients with low HDL-c and/or high triglycerides and average LDL-c concentrations: focus on HDL subpopulations, oxidized LDL, adiponectin, and uric acid. The Scientific World J, 2013, 1-16.
5. Cohen, D. & Fisher, E. (2013). Lipoprotein metabolism, dyslipidemia and nonalcoholic fatty liver disease. Sem Liver Dis, 33(4), 380-388.
6. Díaz, J. & Liem, A. (2005). Utilidad de la medición de la apolipoproteína B en la práctica clínica. Clin Invest Arterioscl, 7(3), 142-146.
7. Chapman, M., Ginsberg, H., Amarenco, P., Andreotti, F., Borén, J., Catapano, A., et al. (2011). Triglyceride-rich lipoproteins and high-density lipoprotein cholesterol in patients at high risk of cardiovascular disease: evidence and guiadance for management. European Heart J, 32, 1345-1361.
8. Choi, S. & Ginsberg, H. (2011). Increased Very Low Density Lipoprotein secretion, hepatic steatosis, and insulin resistance. Trends Endocrinol Metab, 22(9), 353-363.
9. Klop, B., Willem, J. & Castro-Cabezas, M. (2013). Dyslipidemia in obesity: mechanisms and potential targets. Nutrients, 5, 1218-1240.
10. Welty, F. (2013). How do elevated triglycerides and low HDL-cholesterol affect inflammation and atherothrombosis? Curr Cardiol Rep, 15(9), 378-400.
11. Vergés, B. (2015). Pathophysiology of diabetic dyslipidaemia: where are we? Diabetología, 58, 886-899.
12. Daniels, T., Killinger, K., Michal, J., Wright, R. & Jiang, Z. (2009). Lipoproteins, cholesterol homeostasis and cardiac health. Int J Biol Sciences, 5(5), 474-488.
13. Nakajima, K., Nakano, T., Tokita, Y., Nagamine, T., Inazu, A., Kobayashi, J., et al. (2011). Postprandial lipoprotein metabolism; VLDL vs chylomicrons. Clin Chem Acta, 412(15-16), 1306-1318.
14. Enkhmaa, B., Ozturk, Z., Anuurad, E. & Berglund, L. (2010). Postprandial lipoproteins and cardiovascular disease risk in diabetes mellitus. Curr Diab Rep, 10, 61-69.
15. Carey, V., Bishop, L., Laranjo, N., Harshfield, B., Kwiat, C. & Sacks, F. (2010). Controbution of high plasma triglycerides and low High-Density Lipoprotein cholesterol to residual risk of coronary heart disease after establishment of Low-Density Lipoprotein cholesterol control. Am J Cardiol, 106(6), 757-763.
16. Wan, K., Zhao, J., Huang, H., Zhang, Q., Chen, X., Zeng, Z., et al. (2015). The association between Triglyceride/High Density Lipoprotein cholesterol ratio and all-cause mortality in acute coronary syndrome after coronary revascularization. PLoS ONE, 10(4), 1-11.
17. Talayero, B. & Sacks, F. (2011). The role of triglycerides in atherosclerosis. Curr Cardiol Rep, 13(6), 544-552.
18. Bitzur, R., Cohen, H., Kamari, Y., Shaish, A. & Harats, D. (2009). Triglycerides an HDL cholesterol. Diabetes Care, 32, Supplement 2, S373-S377.
19. Kannel, W. & Vasan, R. (2009). Triglycerides as vascular risk factors: new epidemiologic insights for current opinion in cardiology. Curr Opin Cardiol, 24(4), 345-350.
20. Luo, M. & Peng, D. (2016). The emerging role of apolipoprotein C-III: beyond effects on triglyceride metabolism. Lipids in Health and Disease, 15, 1-7.
21. Han, S. H., Nicholls, S., Sakuma, I., Zhao, D. & Koh, K. K. (2016). Hipertriglyceridemia and cardiovascular diseases: revisited. Korean Circulation J, 46(2), 135-144.
22. katsanos, C. (2014). Clinical considerations and mechanistic Determinants of posprandial lipemia in older adults. Adv Nutrition, 5, 226-234.
23. Dallinga-Thie, G., Kroon, J., Borén, J. & Chapman, M. (2016). Triglyceride-rich lipoproteins and remnants: targets for therapy. Curr Cardiol Rep, 18, 1-9.
24. Golberg, I., Eckel, R. & McPherson, R. (2011). Triglycerides and heart disease, still a hypothesis? Arterioscler Thromb Vasc Biol, 31(8), 1716-1725.
25. Boren, J., Matikainen, N., Adiels, M. & Taskinen, M. R. (2014). Postprandial hypertriglyceridemia as a coronary risk factor. Clin Chim Acta, 431, 31–42.
26. Rapp, J. H., Lespine, A., Hamilton, R. L., Colyvas, N., Chaumeton, A. H., Tweedie-Hardman, J., et al. (1994). Triglyceriderich lipoproteins isolated by selected-affinity anti-apolipoprotein B immunosorption from human atherosclerotic plaque. Arterioscler Thromb Vasc Biol, 14, 1767–1774.
27. Daugherty, A., Lange, L. G., Sobel, B. E. & Schonfeld, G (1985). Aortic accumulation and plasma clearance of b-VLDL and HDL: effects of diet-induced hypercholesterolemia in rabbits. J Lipid Res, 26, 955–963.
28. Proctor, S. D. & Mamo, J. C. L. (1998). Retention of fluorescent-labelled chylomicron remnants within the intima of the arterial wall—evidence that plaque cholesterol may be derived from post-prandial lipoproteins. Eur J Clin Invest, 28, 497–504.
29. Wang, L., Gill, R., Pedersen, T., Higgins, L., Newman, J. & Rutledge, J. C. (2009). Triglyceride-rich lipprotein lipolysis releases neutral and oxidized FFAs that induce endothelial cell inflammation. J Lipid Research, 50, 204-213.
30. den Hartigh, L., Altman, R., Norman, J. & Rutledge, J. C. (2013). Posprandial VLDL lipolysis products increase monocyte adhesion and lipid droplet formation via activation of ERK2 and NFkB. Am J Physiol Heart Circ Physiol, 306, H109-H120.
31. Qamar, A., Khetarpal, S., Khera, A., Qasim, A., Rader, D. & Reilly, M. (2015). Plasma Apo C-III levels, triglycerides, and coronary artery calcification in type 2 diabetics. Arterioscler Thromb Vasc Biol, 35(8), 1880-1888.
32. Sacks, F. (2015). The crucial roles of Apolipoproteins E and C-III in ApoB lipoprotein metabolism in normolipidemia and hypertriglyceridemia. Curr Opin Lipidol, 26(1), 56-63.
33. Zheng, C., Khoo, C., Furtado, J. & Sacks, F. (2010). Apolipoprotein Hypertriglyceridemia and the dense Low-Density Lipoprotein phenotype. Circulation, 121(5), 1722-1734.
34. Gordts, P., Nock, R., Son, N. H., Ramms, B., Lew, I., Gonzales, J., et al. (2016). ApoC-III inhibits clearance of triglyceride-rich lipoproteins through LDL family receptors. J Clin Invest, 126(8), 2855-2866.
35. Tran-Dinh, A., Diallo, D., Delbosc, S., Varela-Pérez, M., Dang, Q. B., Lapergue, B., et al. (2013). HDL and endothelial Protection. British J Pharmacology, 169, 493-511.
36. Norata, G. & Catapano, A. (2005). Molecular mechanisms responsible for the antiinflammatory and protective effect of HDL on the endothelium. Vasc Health and Risk Management, 1(2), 119-129.
37. Yuhanna, I. S., Zhu, B. E., Cox, L., Hahner, S., Osborne-Lawrence, P., Lu, Y. L., et al. (2001). High-density lipoprotein binding to scavenger receptor-BI activates endothelial nitric oxide synthase. Nat Med, 7, 853-857.
38. Athyros, V., Tziomalos, K., Karangiannis, A. & Mikhailidis, D. (2011). Dyslipidaemia of obesity, metabolic syndrome and type 2 diabetes mellitus: the case for residual risk reduction after statin treatment. Open Cardiovasc Med J, 5, 24-34.
39. Shinkai, H. (2012). Cholesterol ester transfer-protein modulator and inhibitors and their potential for the treatment of cardiovascular diseases. Vascular health and risk management, 8, 323-331.
40. Jung, U. J. & Choi, M. S. (2014). Obesity and its metabolic complications: the role of adipokines and the relationship between obesity, nonalcoholic fatty liver disease. Int J Mol Sci, 15, 6184-6223.
41. Magkos, F., Mohammed, S. & Mittendorfer, B. (2008). Effect of obesity on the plasma lipoprotein subclass profile in normoglycemic and normolipidemic men and women. Int J Obes (Lond), 32(11), 1655-1664.
42. Liu, M., Chung, S., Shelness, G. & Parks, J. (2012). Hepatic ABCA1 and VLDL triglyceride production. Biochim Biophys Acta, 1821(5), 770-777.
43. Carmena, R., Duriez, P. & Fruchart, J. (2004). Atherogenic lipoprotein particles in atherosclerosis. Circulation, 15, III-2 – III-7.
44. Nikolic, D., Katsiki, N., Montalto, G., Isenovic, E., Mikhailidis, D. & Rizzo, M. (2013). Lipoprotein subfraction in metabolic syndrome and obesity: clinical significance and therapeutic approaches. Nutrients, 5, 928-948.
Publicado
2020-11-13
Número
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Revisiones de literatura
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La propiedad intelectual de los trabajos aceptados es de sus autores, no obstante el acceso a ellos es totalmente abierto y gratuito, por lo que podrán ser reproducidos total o parcialmente con la única limitación de reconocer la autoría y la fuente de publicación ( Revista Medicina Legal de Costa Rica), siempre y cuando dicha explotación no tenga carácter comercial.
Cómo citar
LOS TRIGLICÉRIDOS Y LA ATEROGÉNESIS. (2020). Medicina Legal De Costa Rica, 34(2). https://www.binasss.sa.cr/ojssalud/index.php/mlcr/article/view/73
