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>Journals >Cirugía y Cirujanos >Year 2011, Issue 2

González-Chávez A, Elizondo-Argueta S, Gutiérrez-Reyes G, León-Pedroza JI
Pathophysiological implications between chronic inflammation and the development of diabetes and obesity
Cir Cir 2011; 79 (2)

Language: Español
References: 51
Page: 209-216
PDF: 333.03 Kb.

[Full text - PDF]


The different theories about the mechanisms involved in the development of metabolic disease and its complications converge in the presence of an etiologic chronic proinflammatory state. Chronic inflammation is, at present, the central pathophysiological mechanism involved in the genesis of metabolic diseases. The multiple interactions between the immune system, adipose tissue, the vascular wall and the pancreas are the issues addressed in this review, focusing on specific intracellular and molecular aspects that may become new therapeutic targets. These lead to a proinflammatory, prothrombotic state as well as to proapoptotic endothelial damage that allows the development of atherosclerosis and, consequently, cardiovascular disease. The multiple immunopathological processes associated with the etiology and pathophysiology of different chronic diseases is still in the process of being fully elucidated, allowing the development of new therapeutic targets.

Key words: Chronic inflammation, diabetes, obesity, innate immunity.


  1. Rocha e Silva M. A brief survey of the history of inflammation. Inflamm Res 1978;8:45-49.

  2. Devaraj S, Rosenson R, Jialal I. Metabolic syndrome: an apprasial of the pro-inflammatory and procoagulant status. Endocrinol Metabol Clin 2004;33:431-453.

  3. González CA, Malanco HL, Sánchez ZM, Elizondo AS, Navarro ZJ, Rosillo RS. Inflamación y resistencia a la insulina: mecanismos para el desarrollo de la disfunción endotelial y ateroesclerosis. Rev Mex Cardiol 2006;17:71-82.

  4. Blasi C. The autoimmune origin of atherosclerosis. Atherosclerosis 2008;201:17-32.

  5. Monaco C, Gregan SM, Navin TJ, Foxwell BM, Davies AH, Feldmann M. Toll-like receptor-2 mediates inflammation and matrix degradation in human atherosclerosis. Circulation 2009;120:2462-2469.

  6. Libby P, Ridker PM, Maseri A. Inflammation and atherosclerosis. Circulation 2002;105:1135-1143.

  7. Tabas I. Macrophage death and defective inflammation resolution in atherosclerosis. Nat Rev Immunol 2010;10:36-46.

  8. Mohanty P, Hamouda W, Garg R, Aljada A, Ghanim H, Dandona P. Glucose challenge stimulates reactive oxygen species (ROS) generation by leucocytes. J Clin Endocrinol Metab 2000;85:2970- 2973.

  9. Nappo F, Esposito K, Cioffi M, Giugliano G, Molinari AM, Paolisso G, et al. Postprandial endothelial activation in healthy subjects and type 2 diabetic patients: role of fat and carbohydrate meals. J Am Coll Cardiol 2002;39:1145-1450.

  10. Paravicini TM, Toutz RM. NADPH oxidases, reactive oxygen species, and hypertension: clinical implications and therapeutic possibilities. Diabetes Care 2008;31(suppl 2):S170-180.

  11. Mohanty P, Ghanim H, Hamouda W, Aljada A, Garg R, Dandona P. Both lipid and protein intakes stimulate increased generation of reactive oxygen species by polymorphonuclear leukocytes and mononuclear cells. Am J Clin Nutr 2002;75:762-767.

  12. Ceriello A, Taboga C, Tonutti L, Quagliaro L, Piconi L, Bais B, et al. Evidence for an independent and cumulative effect of postprandial hypertriglyceridemia and hyperglycaemia on endo thelial dysfunction and oxidative stress generation. Circulation 2002;106:1211-1218.

  13. Dandona P, Ghanim H, Chaudhuri A, Dhindsa S, Kim SS. Macronutrient intake induces oxidative and inflammatory stress: potential relevance to atherosclerosis and insulin resistance. Exp Mol Med 2010;42:245-253.

  14. González-Chávez A, Lavalle-González FJ, Elizondo-Argueta S. Conceptos actuales, criterios diagnósticos y algunas consideraciones sobre la fisiopatología del síndrome metabólico. En: González-Chávez A, Lavalle-González FJ, Ríos-González JJ, eds. Síndrome Metabólico y Enfermedad Cardiovascular. Libro 2 con Aplicaciones a la Práctica Clínica. México: Intersistemas; 2006. pp. 7-21.

  15. Mathiew P, Pibarot P, Després JP. Metabolic syndrome: the danger signal in atherosclerosis. Vasc Risk Man 2006;2:285-302.

  16. Miranda PJ, DeFronzo RA, Califf RM, Guyton JR. Metabolic syndrome: definition, pathophysiology and mechanisms. Am Heart J 2005;149:33-45.

  17. Liby P, Okamoto Y. Inflammation in atherosclerosis: transition from theory to practice. Circ J 2010;74:213-220.

  18. Xu H, Barnes GT, Yang Q, Tan G, Yang D, Chou CJ et al. Chronic inflammation in fat plays a crucial role in the development of obesity related insulin resistance. J Clin Invest 2003;112:1821-1830.

  19. Hotamisligil GS. Inflammation and metabolic disorders. Nature 2006;44:860-867.

  20. Hesameddin S, Ali Boroumand MA. Expanded network of inflammatory markers of atherogenesis: where are we now? Open Cardiovasc Med J 2010;4:38-44.

  21. Hirosumi J, Tuncman G, Chang L, Görgün CZ, Uysal KT, Maeda K, et al. A central role for JNK in obesity and insulin resistance. Nature 2002;420:333-340.

  22. Arkan MC. IKK-beta links inflammation to obesity-induced insulin resistance. Nat Med 2005;11:191-198.

  23. De Luca C, Olefsky JM. Inflammation and insulin resistance. FEBS 2008;582:97-105.

  24. Hartge M, Kintscher U, Unger T. Endothelial dysfunction and its role in diabetic vascular disease. Endocrinol Metab Clin North Am 2006;35:551-560.

  25. Hsueh W, Lyon C, Quiñones M. Insulin resistance and the endothelium. Am J Med 2004;117:235-241.

  26. Hartge MM, Kintscher U, Unger T. Endothelial dysfunction and its role in diabetic vascular disease. Endocrinol Metab Clin North Am 2006;35:551-560

  27. González MA, Selwyn AP. Endothelial function, inflammation, and prognosis in cardiovascular disease. Am J Med 2003;115:99-106.

  28. Weisberg SP. CCR2 modulates inflammatory and metabolic effects of high-fat feeding. J Clin Invest 2006;116:115-124.

  29. Kanda H. MCP-1 contributes to macrophage infiltration into adipose tissue, insulin resistance, and hepatic steatosis in obesity. J Clin Invest 2006;116:1494-1505.

  30. Ikeoka D, Mader JK, Pieber. Adipose tissue, inflammation and cardiovascular disease. Rev Assoc Med Bras 2010;56:116-121.

  31. Semple RK, Chatterjee KK. PPARγ and human metabolic disease. J Clin Invest 2006;116:581-589.

  32. Sharma AM, Staels B. Review: Peroxisome proliferator-activated receptor γ and adipose tissue-understanding obesity-related changes in regulation of lipid and glucose metabolism. J Clin Endocrinol Metab 2007;92:386-395.

  33. Tsuchida A, Yamauchi T, Takekawa S, Hada Y, Ito Y, Maki T. Peroxisome proliferator-activated receptor (PPAR)γ activation increases adiponectin receptors and reduces obesity-related inflammation in adipose tissue: comparison of activation of PPARγ , PPARγ and their combination. Diabetes 2005;54:3358-3370.

  34. Chawla A, Barak Y, Nagy L, Liao D, Tontonoz P, Evans RM. PPARgamma dependent and independent effects on macrophage-gene expression in lipid metabolism and inflammation. Nat Med 2001;7:48-52.

  35. Chawla A, Boisvert WA, Lee CH, Laffitte BA, Barak Y, Joseph SB, et al. A PPAR gamma-LXR-ABCA 1 pathway in macrophages is involved in cholesterol efflux and atherogenesis. Mol Cell 2001;7:161-171.

  36. Takeda K, Akira S. Toll-like receptors in innate immunity. Int Immuunol 2005;17:1-14.

  37. Shi H, Kokoeva MV, Inouye K, Tzameli I, Yin H, Flier JS. TLR4 links innate immunity and fatty acid-induced insuline resistance. J Clin Invest 2006;116:3015-3025.

  38. De Kleijn D, Pasterkamp G. Toll-like receptors in cardiovascular diseases. Cardiovasc Res 2003;60:58-67.

  39. Geng H, Wang A, Rong G, Zhu B, Deng Y, Chen J, et al. The effects of ox-LDL in human atherosclerosis may be mediated in part via the toll-like receptor 4 pathway. Mol Cell Biochem 2010;342:201-206.

  40. Saikku P, Leinonen M, Mattila K, Ekman MR, Nieminen MS, Mäkelä PH, et al. Serological evidence of an association of a novel Chlamydia, TWAR, with chronic coronary heart disease and acute myocardial infarction. Lancet 1988;2:983-986.

  41. Blanchard T, Bailey R, Holland M, Mabey D. Chlamydia pneumoniae and atherosclerosis. Lancet 1993;341:825.

  42. Fernández-Riejos P, Najib S, Santos-Álvarez J, Martín-Romero C, Pérez-Pérez A, González-Yanes C, et al. Role of leptin in activationof immune cells. Mediators Inflamm 2010;2010:1-8.

  43. Tschopp J, Schroder K. NLRP3 inflammasome activation: the convergence of multiple signaling pathways on ROS production? Nat Rev Immunol 2010;10:210-215.

  44. Zhou R, Tardivel A, Thorens B, Choi I, Tschopp J. Thioredoxin-interactive protein links oxidative stress to inflammasome activation. Nat Immunol 2010;11:136-141.

  45. Minn AH. Hafele C. Shalev A. Thioredoxin-interacting protein is stimulated by glucose through a carbohydrate response element and induces beta cell apoptosis. Endocrinology 2005;146:2397-2405.

  46. Chen J, Saxena G, Mungrue I, Lusis AJ, Shalev A. Thioredoxininteracting protein: a critical link between glucose toxicity and beta cell apoptosis. Diabetes,2008;57:938-944.

  47. Borradeile NM. Disruption of endoplasmic reticulum structure and integrity in lipotoxic cell death. J Lipid Res 2006;47:2726-2737.

  48. Kharroubi I, Ladriére L, Cardozo A. Dogusan Z, Cnop M, Eizirik D. Free fatty acids and cytokines induce pancreatic β-cell apoptosis by different mechanisms: role of nuclear factor k-β and endoplasmic reticulum stress. Endocrinology 2004;145:5087-5096.

  49. Fulda S. Gorman A, Hori O, Smalli A. Cellular stress responses: cell survival and cell death. Int J Cell Biol 2010;2010:1-23.

  50. Gregor MF, Hotamisligil GS. Adipocyte stress: the endoplasmic reticulum and metabolic disease. J Lipid Res 2007;48:1905-1914.

  51. Lockshin RA, Zakeri Z. Cell death in health and disease. J Cell Mol Med 2007;11:1214-1224.

>Journals >Cirugía y Cirujanos >Year 2011, Issue 2

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