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2015, Número 4

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Rev Mex Anest 2015; 38 (4)


La memoria metabólica y las complicaciones cardiovasculares en el paciente diabético

Luna-Ortiz P, Flores-Chávez PL, Guarner-Lans V, Machado-Diaz AM, Olivares-Sanromán ME, Martínez-Rosas M

Idioma: Español
Referencias bibliográficas: 98
Paginas: 249-263
Archivo PDF: 437.26 Kb.


RESUMEN

La diabetes mellitus se considera una pandemia en la actualidad y es una enfermedad comúnmente encontrada durante la anestesia. Representa un factor de riesgo independiente de morbimortalidad en cirugías mayores. En la actualidad, las herramientas farmacológicas con las que contamos no son suficientes para detener y revertir las alteraciones vasculares propias de la DM, en particular las microvasculares. La evaluación integral del paciente diabético debe considerar la historia de la enfermedad y en particular la presencia de la memoria metabólica que se define como el efecto a largo plazo de un estado hiperglucémico prolongado previo que lleva al desarrollo de las complicaciones vasculares. Estudios aleatorizados a gran escala han demostrado que el control intensivo temprano de la glucemia puede reducir la incidencia y progresión de las complicaciones micro- y macrovasculares en estos pacientes mientras que los períodos de hiperglucemia crónica debido a un mal control, principalmente durante las etapas iniciales de la diabetes, dejan una marca celular que permite el desarrollo y la progresión de las complicaciones vasculares, incluso cuando se alcanza el control euglucémico. Por lo tanto, la memoria metabólica es una condición que puede explicar las complicaciones vasculares en los resultados quirúrgicos a corto y a largo plazo. En esta revisión, ofrecemos al anestesiólogo una visión general del fenómeno describiendo sus posibles mecanismos fisiopatológicos a nivel celular y molecular y discutiendo las implicaciones terapéuticas para el manejo de esta condición.


REFERENCIAS (EN ESTE ARTÍCULO)

  1. Sudhakaran S, Surani SR. Guidelines for perioperative management of the diabetic patient. Surg Res Pract. 2015;2015:284063. doi: 10.1155/2015/284063.

  2. World Health Organization. Noncommunicable diseases country profiles 2014. WHO global report. Available in: http://www.who.int/nmh/countries/en/

  3. Duncan AE. Hyperglycemia and perioperative glucose management. Curr Pharm Des. 2015;18:6195-6203.

  4. Stevanovic K, Sabljak V, Toskovic A, et al. Anaesthesia and the patient with diabetes. Diabetes Metab Syndr. 2015;9:177-179.

  5. Subramaniam B, Pomposelli F, Talmor D, et al. Perioperative and long-term morbidity and mortality after above-knee and below-knee amputations in diabetics and nondiabetics. Anesth Analg. 2005;100:1241-1247.

  6. Cook G, Gall I. Anaesthetic management of the patient with diabetes. Anaesthesia & Intensive Care Medicine. 2011;12:438-441.

  7. Writing Team for the Diabetes Control and Complications/Epidemiology of Diabetes Interventions and Complications Research Group. Effect of intensive therapy on the microvascular complications of type 1 diabetes mellitus. JAMA. 2002;87:2563-2569.

  8. Writing Team for the Diabetes Control and Complications/Epidemiology of Diabetes Interventions and Complications Research Group. Sustained effect of intensive treatment of type 1 diabetes mellitus on development and progression of diabetic nephropathy: the Epidemiology of Diabetes Interventions and Complications (EDIC) study. JAMA. 2003;290:2159-2167.

  9. Nathan DM, Cleary PA, Backlund JY, et al; Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications (DCCT/EDIC) Study Research Group. Intensive diabetes treatment and cardiovascular disease in patients with type 1 diabetes. N Engl J Med. 2005;353:2643-2653.

  10. Nathan DM, Lachin J, Cleary PA, et al; Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications (DCCT/EDIC) Study Research Group. Intensive diabetes therapy and carotid intima-media thickness in type 1 diabetes mellitus. N Engl J Med. 2003;348:2294-2303.

  11. Holman RR, Paul SK, Bethel MA, et al. 10-year follow-up of intensive glucose control in type 2 diabetes. N Engl J Med. 2008;359:1565-1576.

  12. Wright AD. Metabolic memory in type 1 diabetes. Br J Diabetes Vasc Dis. 2009;9:254-257.

  13. Ceriello A, Ihnat MA, Thorpe JE. The “metabolic memory”- is more than just tight glucose control necessary to prevent diabetic complications? J Clin Endocrinol Metab. 2009;94:410-415.

  14. Rahbar S, Natarajan R, Yerneni K, et al. Evidence that pioglitazone, metformin and pentoxifylline are inhibitors of glycation. Clin Chim Acta. 2000;301:65-77.

  15. Miyata T, van Ypersele de Strihou C, Ueda Y, et al. Angiotensin II receptor antagonists and angiotensin-converting enzyme inhibitors lower in vitro the formation of advanced glycation end products: biochemical mechanisms. J Am Soc Nephrol. 2002;13:2478-2487.

  16. Yoshida T, Yamagishi S, Nakamura K, et al. Telmisartan inhibits AGE-induced C-reactive protein production through down regulation of the receptor for AGE via peroxisome proliferator-activated receptor-gamma activation. Diabetología. 2006;49:3094-3099.

  17. Ceriello A, Assaloni R, Da Ros R, 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. 2005;111:2518-2524.

  18. Ceriello A, Piconi L, Esposito K, et al. Telmisartan shows an equivalent effect of vitamin C in further improving endothelial dysfunction after glycemia normalization in type 1 diabetes. Diabetes Care. 2007;30:1694-1698.

  19. Corgnali M, Piconi L, Ihnat M, et al. Evaluation of gliclazide ability to attenuate the hyperglycaemic “memory” induced by high glucose in isolated human endothelial cells. Diabetes Metab Res Rev. 2007;24:301-309.

  20. Hammes HP, Du X, Edelstein D, et al. Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy. Nat Med. 2003;9:294-299.

  21. Du X, Edelstein D, Brownlee M. Oral benfotiamine plus alpha-lipoic acid normalises complication-causing pathways in type 1 diabetes. Diabetología. 2008;51:1930-1932.

  22. Takigawa-Imamura H, Sekine T, Murata M, et al. Stimulation of glucose uptake in muscle cells by prolonged treatment with scriptide, a histone deacetylase inhibitor. Biosci Biotechnol Biochem. 2003;67:1499-1506.

  23. Galmozzi A, Mitro N, Ferrari A, et al. Inhibition of class I histone deacetylases unveils a mitochondrial signature and enhances oxidative metabolism in skeletal muscle and adipose tissue. Diabetes. 2013;62:732-742.

  24. Crosson CE, Mani SK, Husain S, et al. Inhibition of histone deacetylase protects the retina from ischemic injury. Invest Ophthalmol Vis Sci. 2010;51:3639-3645.

  25. Lenoir O, Flosseau K, Ma FX, et al. Specific control of pancreatic endocrine beta- and delta-cell mass by class IIa histone deacetylases HDAC4, HDAC5, and HDAC9. Diabetes. 2011;60:2861-2871.

  26. Engerman RL, Kern TS. Progression of incipient diabetic retinopathy during good glycemic control. Diabetes. 1987;36:808-812.

  27. Roy S, Sala R, Cagliero E, et al. Overexpression of fibronectin induced by diabetes or high glucose: phenomenon with a memory. Proc Natl Acad Sci USA. 1990;87:404-407.

  28. Hammes HP, Klinzing I, Wiegand S, et al. Islet transplantation inhibits diabetic retinopathy in the sucrose-fed diabetic rat. Invest Ophthalmol Vis Sci. 1993;34:2092-2096.

  29. The Diabetes Control and Complications Trial Research Group. The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus. N Engl J Med. 1993;329:977-986.

  30. Ceriello A, Esposito K, Ihnat M, et al. Long-term glycemic control influences the long-lasting effect of hyperglycemia on endothelial function in type 1 diabetes. J Clin Endocrinol Metab. 2009;94:2751-2756.

  31. King P, Peacock I, Donnelly R. The UK prospective diabetes study (UKPDS): clinical and therapeutic implications for type 2 diabetes. Br J Clin Pharmacol. 1999;48:643-648.

  32. Holman RR, Paul SK, Bethel MA, et al. 10-year follow-up of intensive glucose control in type 2 diabetes. N Engl J Med. 2008;359:1565-1576.

  33. Lucas A. Programming by early nutrition. An experimental approach. J Nutr. 1998;28:401S-406S.

  34. Aalinkeel R, Srinivasan M, Kalhan SC, et al. A dietary intervention (high carbohydrate) during the neonatal period causes islet dysfunction in rats. Am J Physiol. 1999;277:E1061-E1069.

  35. Srinivasan M, Aalinkeel R, Song F, et al. Maternal hyperinsulinemia predisposes rat fetuses for hyperinsulinemia, and adult-onset obesity and maternal mild food restriction reverses this phenotype. Am J Physiol Endocrinol Metab. 2006;290:E129-E134.

  36. Leduc L, Levy E, Bouity-Voubou M, et al. Fetal programming of atherosclerosis: possible role of the mitochondria. Eur J Obstet Gynecol Reprod Biol. 2010;149:127-130.

  37. Thompson JA, Webb RC. Potential role of Toll-like receptors in programming of vascular dysfunction. Clin Sci (Lond). 2013;125:19-25.

  38. Sies H. Oxidative stress: oxidants and antioxidants. New York: Academic Press; 1991.

  39. Halliwell B, Whiteman M. Measuring reactive species and oxidative damage in vivo and in cell culture: how should you do it and what do the results mean? Br J Pharmacol. 2004;142:231-255.

  40. Martin-Gallan P, Carrascosa A, Gussinye M, et al. Biomarkers of diabetes-associated oxidative stress and antioxidant status in young diabetic patients with or without subclinical complications. Free Radic Biol Med. 2003;34:1563-1574.

  41. Varvarovska J, Racek J, Stozicky F, et al. Parameters of oxidative stress in children with type 1 diabetes mellitus and their relatives. J Diabetes Complications. 2003;17:7-10.

  42. VanderJagt DJ, Harrison JM, Ratliff DM, et al. Oxidative stress indices in IDDM subjects with and without long-term diabetic complications. Clin Biochem. 2001;34:265-270.

  43. Dalle-Donne I, Rossi R, Colombo R, et al. Biomarkers of oxidative damage in human disease. Clinical Chemistry. 2006;52:601-623.

  44. Wold LE, Ceylan-Isik AF, Ren J. Oxidative stress and stress signaling: menace of diabetic cardiomyopathy. Acta Pharmacol Sin. 2005;26:908-917.

  45. Mohanty P, Hamouda W, Gang R, et al. Glucose challenge stimulates reactive oxygen species (ROS) generation by leucocytes. J Clin Endocrinol Metab. 2000;85:2970-2973.

  46. Korshunov SS, Skulachev VP, Starkov AA. High protonic potential actuates a mechanism of production of reactive oxygen species in mitochondria. FEBS Lett. 1997;416:15-18.

  47. Ceriello A, Mercuri F, Quagliaro L, et al. Detection of nitrotyrosine on the diabetic plasma: evidence of oxidative stress. Diabetología. 2001;4:834-838.

  48. Ceriello A, Esposito K, Ihnat M, et al. Long-term glycemic control influences the long-lasting effect of hyperglycemia on endothelial function in type 1 diabetes. J Clin Endocrinol Metab. 2009;94:2751-2756.

  49. Kowluru RA. Effect of reinstitution of good glycemic control on retinal oxidative stress and nitrative stress in diabetic rats. Diabetes. 2003;52:818-823.

  50. Kowluru RA, Koppolu P. Termination of experimental galactosemia in rats, and progression of retinal metabolic abnormalities. Invest Ophthalmol Visc Sci. 2002;43:3287-3291.

  51. Kowluru RA, Kanwar M, Kennedy A. Metabolic memory phenomenon and accumulation of peroxynitrite in retinal capillaries. Exp Diabetes Res. 2007;2007:21976.

  52. Dunn KC, Aotaki-Keen AE, Putkey FR, et al. ARPE-19, a human retinal pigment epithelial cell line with differentiated properties. Exp Eye Res. 1996;62:155-169.

  53. Schisano B, Tripathi G, McGee K, et al. Glucose oscillations, more than constant high glucose, induce p53 activation and a metabolic memory in human endothelial cells. Diabetologia. 2011;54:1219-1226.

  54. Tesfamariam B, Brown ML, Cohen RA. Elevated glucose impairs endothelium-dependent relaxation by activating protein kinase C. J Clin Invest. 1991;87:1643-1648.

  55. Brownlee M. The pathobiology of diabetic complications: a unifying mechanism. Diabetes. 2005;54:1615-1625.

  56. Brownlee M. Biochemistry and molecular cell biology of diabetic complications. Nature. 2001;414:813-820.

  57. Li JM, Shah AM. Endothelial cell superoxide generation: regulation and relevance for cardiovascular pathophysiology. Am J Physiol Regul Integr Comp Physiol. 2004;287:R1014-R1030.

  58. Giacco F, Brownlee M. Oxidative stress and diabetic complications. Circ Res. 2010;107:1058-1070.

  59. Nishikawa T, Edelstein D, Du XL, et al. Normalizing mitocondrial superoxide production blocks three pathways of hyperglycaemic damage. Nature. 2000;404:787-790.

  60. Wallace DC. Diseases of the mitochondrial DNA. Annu Rev Biochem. 1992;61:1175-1212.

  61. Green K, Brand MD, Murphy MP. Prevention of mitochondrial oxidative damage as a therapeutic strategy in diabetes. Diabetes. 2004;53:S110-S118.

  62. Sivitz WI, Yorek MA. Mitochondrial dysfunction in diabetes: from molecular mechanisms to functional significance and therapeutic opportunities. Antiox Redox Signal. 2010;12:537-577.

  63. Goldin A, Beckman JA, Schmidt AM, et al. Advanced glycation end-products: sparking the development of diabetic vascular injury. Circulation. 2006;114:597-605.

  64. Maillard LC. Action of amino acids on sugars. Formation of melanoidins in a methodical way. Compt Rend. 1912;54:66-68.

  65. Meerwaldt R, Graaff R, Oomen PH, et al. Simple non-invasive assessment of advanced glycation end product accumulation. Diabetologia. 2004;47:1324-1330.

  66. Stirban A, Gawlowski T, Roden M. Vascular effects of advanced glycation end products: clinical effects and molecular mechanisms. Molecular Metabolism. 2014;3:94-108.

  67. Monnier VM, Bautista O, Kenny D, et al. Skin collagen glycation, glycoxidation, and crosslinking are lower in subjects with long-term intensive versus conventional therapy of type 1 diabetes: relevance of glycated collagen products versus HbA1c as markers of diabetic complications. DCCT Skin Collagen Ancillary Study Group. Diabetes Control and Complications Trial. Diabetes. 199;48:870-880.

  68. Schmidt AM, Hori O, Brett J, et al. Cellular receptors for advanced glycation end products. Implications for induction of oxidant stress and cellular dysfunction in the pathogenesis of vascular lesions. Arterioscler Thromb. 1994;14:1521-1528.

  69. Zong H, Ward M, Stitt AW. AGEs, RAGE, and diabetic retinophaty. Curr Diab Rep. 2001;11:244-245.

  70. Semenkovich CF, Heinecke JW. The mystery of diabetes and atherosclerosis. Diabetes. 1997;46:327-344.

  71. Aronson D, Rayfield EJ. How hyperglycemia promotes atherosclerosis: molecular mechanisms. Cardiovasc Diabetol. 2002;1:1.

  72. Rosca MG, Mustata TG, Kinter MT, et al. Glycation of mitochondrial proteins from diabetic rat kidney is associated with excess superoxide formation. Am J Physiol. 2005;289:F420-F430.

  73. Waddington CH. Der epigenotypus. Endeavour. 1942;1:18-20.

  74. Holliday R. The inheritance of epigenetic defects. Science. 1987;238:63-170.

  75. Meagher RB, Müssar JK. The influence of DNA sequence on epigenome induced pathologies. Epigenetics & Chromatin. 2012;5:11. doi: 10.1186/1756-8935-5-11.

  76. Keating S, El-Osta A. Epigenetic changes in diabetes. Clin Genet. 2013;84:1-10.

  77. Brasacchio D, Okabe J, Tikellis C, et al. Hyperglycemia induces a dynamic cooperativity of histone methylase and demethylase enzymes associated with gene-activating epigenetic marks that coexist on the lysine tail. Diabetes. 2009;58:1229-1236.

  78. El Osta A, Brasacchio D, Yao D, et al. Transient high glucose causes persistent epigenetic changes and altered gene expression during subsequent normoglycemia. J Exp Med. 2008;205:2409-2417.

  79. Siebel AL, Fernandez AZ, El-Osta A. Glycemic memory associated epigenetic changes. Biochem Pharmacol. 2010;80:1853-1859.

  80. Martin C, Zhang Y. The diverse functions of histone lysine methylation. Nat Rev Mol Cell Biol. 2005;6:838-849.

  81. Bird AP. DNA methylation and the frequency of CpG in animal DNA. Nucleic Acids Res. 1980;8:1499-1504.

  82. Meissner A. Epigenetic modifications in pluripotent and differentiated cells. Nat Biotechnol. 2010;28:1079-1088.

  83. Macfarlane AJ, Strom A, Scott FW. Epigenetics: deciphering how environmental factors may modify autoimmune type 1 diabetes. Mamm Genome. 2009;20:624-632.

  84. Stefan M, Zhang W, Concepcion E, et al. DNA methylation profiles in type 1 diabetes twins point to strong epigenetic effects on etiology. J Autoimmun. 2014;50:33-37.

  85. Ribel-Madsen R, Fraga MF, Jacobsen S, et al. Genome-wide analysis of DNA methylation differences in muscle and fat from monozygotic twins discordant for type 2 diabetes. PLoS One. 2012;7:e51302. doi: 10.1371/journal.pone.0051302 7:e51302.

  86. Ventura-Clapier R, Garnier A, Veksler V. Transcriptional control of mitochondrial biogenesis: the central role of PGC-1alpha. Cardiovasc Res. 2008;79:208-217.

  87. Reddy MA, Natarajan R. Epigenetic mechanisms in diabetic vascular complications. Cardiovasc Res. 2011;90:421-429. doi: 10.1093/cvr/cvr024.

  88. Guarner V, Rubio-Ruiz ME. Low-grade systemic inflammation connects aging, metabolic syndrome and cardiovascular disease. Interdiscip Top Gerontol. 2015;40:99-106.

  89. Thompson JA, Webb RC. Potential role of Toll-like receptors in programming of vascular dysfunction. Clin Sci (Lond). 2013;125:19-25.

  90. Nitert MD, Dayeh T, Volkov P, et al. Impact of an exercise intervention on DNA methylation in skeletal muscle from first-degree relatives of patients with type 2 diabetes. Diabetes. 2012;61:3322-3332.

  91. Brasacchio D, Okabe J, Tikellis C, et al. Hyperglycemia induces a dynamic cooperativity of histone methylase and demethylase enzymes associated with gene-activating epigenetic marks that coexist on the lysine tail. Diabetes. 2009;58:1229-1236.

  92. Pirola L, Balcerczyk A, Tothill RW, Haviv I, Kaspi A, Lunke S, et al. Genome-wide analysis distinguishes hyperglycemia regulated epigenetic signatures of primary vascular cells. Genome Res. 2011;21:1601-1615.

  93. Takizawa F, Mizutani S, Ogawa Y, et al. Glucose-independent persistence of PAI-1 gene expression and H3K4 tri-methylation in type 1 diabetic mouse endothelium: implication in metabolic memory. Biochem Biophys Res Commun. 2013;433:66-72.

  94. Vecellio M, Spallotta F, Nanni S, et al. The histone acetylase activator pentadecylidenemalonate 1b rescues proliferation and differentiation in human cardiac mesenchymal cells of type 2 diabetic patients. Diabetes. 2014;63:2132-2147. doi: 10.2337/db13-0731.

  95. Cencioni C, Spallotta F, Martelli F, et al. Oxidative stress and epigenetic regulation in ageing and age-related diseases. Int J Mol Sci. 2013;14:17643-17663.

  96. Lewis EC, Blaabjerg L, Storling J, et al. The oral histone deacetylase inhibitor ITF2357 reduces cytokines and protects islet beta cells in vivo and in vitro. Mol Med. 2011;17:369-377.

  97. Tedong L, Madiraju P, Martineau LC, et al. Hydro-ethanolic extract of cashew tree (Anacardium occidentale) nut and its principal compound, anacardic acid, stimulate glucose uptake in C2C12 muscle cells. Mol Nutr Food Res. 2010;54:1753-1762.

  98. Halili MA, Andrews MR, Labzin LI, Schroder K, Matthias G, Cao C, et al. Differential effects of selective HDAC inhibitors on macrophage inflammatory responses to the Toll-like receptor 4 agonist LPS. J Leukoc Biol. 2010;87:1103-1114




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