2018, Número 3
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Residente 2018; 13 (3)
Conectando la enfermedad de Chagas y la diabetes
Espinoza B, Martínez I
Idioma: Español
Referencias bibliográficas: 64
Paginas: 84-92
Archivo PDF: 286.15 Kb.
RESUMEN
La diabetes es un padecimiento crónico caracterizado por la incapacidad del organismo para producir insulina (diabetes tipo 1, DMT1) o para utilizarla eficientemente (diabetes tipo 2, DMT2). En ambos casos se observan elevadas concentraciones de glucosa en sangre, con el consecuente daño a diversos tejidos. Se ha propuesto que la etiología de la DMT1 está relacionada con fenómenos de autoinmunidad, mientras que la DMT2 tiene su origen en desórdenes metabólicos de los tejidos que responden a la insulina.
Trypanosoma cruzi, el agente causal de la enfermedad de Chagas, tiene la capacidad de infectar múltiples tejidos, incluidos los islotes de Langerhans y el tejido adiposo. En estos sitios, la presencia del parásito puede inducir procesos de autoinmunidad o alteraciones metabólicas que contribuirían al establecimiento del cuadro diabético. Este trabajo presenta una revisión de las evidencias experimentales publicadas hasta el momento.
REFERENCIAS (EN ESTE ARTÍCULO)
Traina M, Meymandi S, Bradfield JS. Heart failure secondary to Chagas disease: an emerging problem in non-endemic areas. Curr Heart Fail Rep. 2016; 13 (6): 295-301.
Hidron AI, Gilman RH, Justiniano J, Blackstock AJ, Lafuente C, Selum W et al. Chagas cardiomyopathy in the context of the chronic disease transition. PLoS Negl Trop Dis. 2010; 4 (5): e688.
Chen LH, Leder K, Barbre KA, Schlagenhauf P, Libman M, Keystone J et al. Business travel-associated illness: a GeoSentinel analysis. J Travel Med. 2018; 25 (1). doi: 10.1093/jtm/tax097.
WHO. Definition and diagnosis of diabetes mellitus and intermediate hyperglycemia, report of a WHO/IDF Consultation. Geneva, Switzerland: World Health Organization Press/International Diabetes Federation; 2006.
Dufurrena Q, Amjad FM, Scherer PE, Weiss LM, Nagajyothi J, Roth J et al. Alterations in pancreatic β cell function and Trypanosoma cruzi infection: evidence from human and animal studies. Parasitol Res. 2017; 116 (3): 827-838.
Peiró C, Romacho T, Azcutia V, Villalobos L, Fernández E, Bolaños JP et al. Inflammation, glucose, and vascular cell damage: the role of the pentose phosphate pathway. Cardiovasc Diabetol. 2016; 15: 82.
INSP. Encuesta Nacional de Salud y Nutrición de Medio Camino 2016. México: Instituto Nacional de Salud Pública; 2017. p. 151.
Liu HW, Xu RY, Sun RP, Wang Q, Liu JL, Ge W et al. Association of PTPN22 gene polymorphism with type 1 diabetes mellitus in Chinese children and adolescents. Genet Mol Res. 2015; 14 (1): 63-68.
Graham KL, Krishnamurthy B, Fynch S, Ayala-Pérez R, Slattery RM, Santamaría P et al. Intra-islet proliferation of cytotoxic T lymphocytes contributes to insulitis progression. Eur J Immunol. 2012; 42 (7): 1717-1722.
Winkler C, Raab J, Grallert H, Ziegler AG. Lack of association of type 2 diabetes susceptibility genotypes and body weight on the development of islet autoimmunity and type 1 diabetes. PLoS One. 2012; 7 (4): e35410.
Reeds J, Mansuri S, Mamakeesick M, Harris SB, Zinman B, Gittelsohn J et al. Dietary patterns and type 2 diabetes mellitus in a first nations community. Can J Diabetes. 2016; 40 (4): 304-310.
Bikman BT, Guan Y, Shui G, Siddique MM, Holland WL, Kim JY et al. Fenretinide prevents lipid-induced insulin resistance by blocking ceramide biosynthesis. J Biol Chem. 2012; 287 (21): 17426-17437.
Jeon CY, Haan MN, Cheng C, Clayton ER, Mayeda ER, Miller JW et al. Helicobacter pylori infection is associated with an increased rate of diabetes. Diabetes Care. 2012; 35 (3): 520-525.
Smelt MJ, Faas MM, de Haan BJ, Draijer C, Hugenholtz GC, de Haan A et al. Susceptibility of human pancreatic β cells for cytomegalovirus infection and the effects on cellular immunogenicity. Pancreas. 2012; 41 (1): 39-49.
OMS. La enfermedad de Chagas (tripanosomiasis americana): Nota descriptiva. Disponible en: http://www.who.int/mediacentre/factsheets/fs340/es/. [Consultado 18 de Marzo de 2017]. Organización Mundial de la Salud; 2017.
Epidemiología: Boletín Epidemiológico, Sistema Nacional de Vigilancia Epidemiológica. México: Secretaría de Salud; 2017.
WHO. First WHO report on neglected tropical diseases 2010: working to overcome the global impact of neglected tropical diseases. Crompton DWT. WHO Press; 2010.
Marin-Neto JA, Rassi A Jr. Update on Chagas heart disease on the first centenary of its discovery. Rev Esp Cardiol. 2009; 62 (11): 1211-1216.
Espinoza B, Rico T, Sosa S, Oaxaca E, Vizcaíno-Castillo A, Caballero ML et al. Mexican Trypanosoma cruzi T. cruzi I strains with different degrees of virulence induce diverse humoral and cellular immune responses in a murine experimental infection model. J Biomed Biotechnol. 2010; 2010: 890672.
Espinoza B, Solórzano-Domínguez N, Vizcaíno-Castillo A, Martínez I, Elías-López AL, Rodríguez-Martínez JA. Gastrointestinal infection with Mexican TcI Trypanosoma cruzi strains: different degrees of colonization and diverse immune responses. Int J Biol Sci. 2011; 7 (9): 1357-1370.
Guarner J, Bartlett J, Zaki SR, Colley DG, Grijalva MJ, Powell MR. Mouse model for Chagas disease: immunohistochemical distribution of different stages of Trypanosoma cruzi in tissues throughout infection. Am J Trop Med Hyg. 2001; 65 (2): 152-158.
Melnikov VG, Velasco FF, Espinoza-Gómez F, Rodríguez FG, Dobrovinskaya OR. Pathologic changes in lungs caused by Mexican isolates of Trypanosoma cruzi in the acute phase of infection in mice. Am J Trop Med Hyg. 2005; 73 (2): 301-306.
Calabrese KS, Lagrange PH, da Costa SC. Trypanosoma cruzi: histopathology of endocrine system in immunocompromised mice. Int J Exp Pathol. 1994; 75 (6): 453-462.
Savino W. The thymic microenvironment in infectious diseases. Mem Inst Oswaldo Cruz. 1990; 85 (3): 255-260.
Ferreira AV, Segatto M, Menezes Z, Macedo AM, Gelape C, de Oliveira-Andrade L et al. Evidence for Trypanosoma cruzi in adipose tissue in human chronic Chagas disease. Microbes Infect. 2011; 13 (12-13): 1002-1005.
dos Santos VM, de Lima MA, Cabrine-Santos M, Márquez D de S, Reis Md, Pereira Gde A et al. Pancreatic hepatocytes in hamsters (Mesocricetus auratus) infected with Trypanosoma cruzi. Exp Parasitol. 2002; 100 (2): 103-111.
Corbett CE, Scremin LH, Lombardi RA, Gama-Rodrigues JJ, Okumura M. Pancreatic lesions in acute experimental Chagas’ disease. Rev Hosp Clin Fac Med Sao Paulo. 2002; 57 (2): 63-66.
Martello LA, Wadgaonkar R, Gupta R, Machado FS, Walsh MG, Mascareno E et al. Characterization of Trypanosoma cruzi infectivity, proliferation, and cytokine patterns in gut and pancreatic epithelial cells maintained in vitro. Parasitol Res. 2013; 112 (12): 4177-4183.
Nagajyothi F, Kuliawat R, Kusminski CM, Machado FS, Desruisseaux MS, Zhao D et al. Alterations in glucose homeostasis in a murine model of Chagas disease. Am J Pathol. 2013; 182 (3): 886-894.
Ramírez LE, Lages-Silva E, Soares-Júnior JM, Chapadeiro E. The hamster (Mesocricetus auratus) as experimental model in Chagas’ disease: parasitological and histopathological studies in acute and chronic phases of Trypanosoma cruzi infection. Rev Soc Bras Med Trop. 1994; 27 (3): 163-169.
Zhang W, Zhao Y, Zeng Y, Yu X, Yao J, Zhao S et al. Hyperlipidemic versus normal-lipid acute necrotic pancreatitis: proteomic analysis using an animal model. Pancreas. 2012; 41 (2): 317-322.
Cunha-Neto E, Teixeira PC, Nogueira LG, Kalil J. Autoimmunity. Adv Parasitol. 2011; 76: 129-152.
Garg N, Popov VL, Papaconstantinou J. Profiling gene transcription reveals a deficiency of mitochondrial oxidative phosphorylation in Trypanosoma cruzi-infected murine hearts: implications in chagasic myocarditis development. Biochim Biophys Acta. 2003; 1638 (2): 106-120.
Tang C, Koulajian K, Schuiki I, Zhang L, Desai T, Ivovic A et al. Glucose-induced beta cell dysfunction in vivo in rats: link between oxidative stress and endoplasmic reticulum stress. Diabetologia. 2012; 55 (5): 1366-1379.
Attie AD, Scherer PE. Adipocyte metabolism and obesity. J Lipid Res. 2009; 50 Suppl: S395-S399.
Combs TP, Nagajyothi, Mukherjee S, de Almeida CJ, Jelicks LA, Schubert W et al. The adipocyte as an important target cell for Trypanosoma cruzi infection. 2005; 280 (25): 24085-24094.
Nagajyothi F, Desruisseaux MS, Machado FS, Upadhya R, Zhao D, Schwartz GJ et al. Response of adipose tissue to early infection with Trypanosoma cruzi (Brazil strain). J Infect Dis. 2012; 205 (5): 830-840.
Wen JJ, Nagajyothi F, Machado FS, Weiss LM, Scherer PE, Tanowitz HB et al. Markers of oxidative stress in adipose tissue during Trypanosoma cruzi infection. Parasitol Res. 2014; 113 (9): 3159-3165.
Nagajyothi F, Desruisseaux MS, Thiruvur N, Weiss LM, Braunstein VL, Albanese C et al. Trypanosoma cruzi infection of cultured adipocytes results in an inflammatory phenotype. Obesity (Silver Spring). 2008; 16 (9): 1992-1997.
Miao Q, Ndao M. Trypanosoma cruzi infection and host lipid metabolism. Mediators Inflamm. 2014; 2014: 902038.
Nagajyothi F, Weiss LM, Silver DL, Desruisseaux MS, Scherer PE, Herz J et al. Trypanosoma cruzi utilizes the host low density lipoprotein receptor in invasion. PLoS Negl Trop Dis. 2011; 5 (2): e953.
Nagajyothi F, Desruisseaux MS, Weiss LM, Chua S, Albanese C, Machado FS et al. Chagas disease, adipose tissue and the metabolic syndrome. Mem Inst Oswaldo Cruz. 2009; 104 Suppl 1: 219-225.
Juan CC, Chuang TY, Chang CL, Huang SW, Ho LT. Endothelin-1 regulates adiponectin gene expression and secretion in 3T3-L1 adipocytes via distinct signaling pathways. Endocrinology. 2007; 148 (4): 1835-1842.
Nagajyothi F, Machado FS, Burleigh BA, Jelicks LA, Scherer PE, Mukherjee S et al. Mechanisms of Trypanosoma cruzi persistence in Chagas disease. Cell Microbiol. 2012; 14 (5): 634-643.
Tanowitz HB, Scherer PE, Mota MM, Figueiredo LM. Adipose tissue: a safe haven for parasites? Trends Parasitol. 2017; 33 (4): 276-284.
Cencig S, Coltel N, Truyens C, Carlier Y. Parasitic loads in tissues of mice infected with Trypanosoma cruzi and treated with AmBisome. PLoS Negl Trop Dis. 2011; 5 (6): e1216.
Ronco MT, Francés DE, Ingaramo PI, Quiroga AD, Álvarez ML, Pisani GB et al. Tumor necrosis factor alpha induced by Trypanosoma cruzi infection mediates inflammation and cell death in the liver of infected mice. Cytokine. 2010; 49 (1): 64-72.
Carrera-Silva EA, Cano RC, Guiñazú N, Aoki MP, Pellegrini A, Gea S. TLR2, TLR4 and TLR9 are differentially modulated in liver lethally injured from BALB/c and C57BL/6 mice during Trypanosoma cruzi acute infection. Mol Immunol. 2008; 45 (13): 3580-3588.
Carrera-Silva EA, Guiñazu N, Pellegrini A, Cano RC, Arocena A, Aoki MP et al. Importance of TLR2 on hepatic immune and non-immune cells to attenuate the strong inflammatory liver response during Trypanosoma cruzi acute infection. PLoS Negl Trop Dis. 2010; 4 (11): e863.
Penas FN, Cevey ÁC, Siffo S, Mirkin GA, Goren NB. Hepatic injury associated with Trypanosoma cruzi infection is attenuated by treatment with 15-deoxy-Δ12,14 prostaglandin J2. Exp Parasitol. 2016; 170: 100-108.
Palhares PE, Fontana Júnior P, Schaffer GM, Marcondes NS, Vergara M. Tissue damage markers in experimental Chagas’ disease. Braz J Med Biol Res. 1988; 21 (5): 957-959.
Sunnemark D, Harris RA, Frostegård J, Orn A. Induction of early atherosclerosis in CBA/J mice by combination of Trypanosoma cruzi infection and a high cholesterol diet. Atherosclerosis. 2000; 153 (2): 273-282.
Cabalén ME, Cabral MF, Sanmarco LM, Andrada MC, Onofrio LI, Ponce NE et al. Chronic Trypanosoma cruzi infection potentiates adipose tissue macrophage polarization toward an anti-inflammatory M2 phenotype and contributes to diabetes progression in a diet-induced obesity model. Oncotarget. 2016; 7 (12): 13400-13415.
Tanowitz HB, Amole B, Hewlett D, Wittner M. Trypanosoma cruzi infection in diabetic mice. Trans R Soc Trop Med Hyg. 1988; 82 (1): 90-93.
Nagajyothi F, Weiss LM, Zhao D, Koba W, Jelicks LA, Cui MH et al. High fat diet modulates Trypanosoma cruzi infection associated myocarditis. PLoS Negl Trop Dis. 2014; 8 (10): e3118.
Brima W, Eden DJ, Mehdi SF, Bravo M, Wiese MM, Stein J et al. The brighter (and evolutionarily older) face of the metabolic syndrome: evidence from Trypanosoma cruzi infection in CD-1 mice. Diabetes Metab Res Rev. 2015; 31 (4): 346-359.
Freitas HF, Barbosa EA, Rosa FH, Lima AC, Mansur AJ. Association of HDL cholesterol and triglycerides with mortality in patients with heart failure. Braz J Med Biol Res. 2009; 42 (5): 420-425.
Geraix J, Ardisson LP, Marcondes-Machado J, Pereira PC. Clinical and nutritional profile of individuals with Chagas disease. Braz J Infect Dis. 2007; 11 (4): 411-414.
dos Santos VM, da Cunha SF, Teixeira V de P, Monteiro JP, dos Santos JA, dos Santos TA et al. Frequency of diabetes mellitus and hyperglycemia in chagasic and non-chagasic women. Rev Soc Bras Med Trop. 1999; 32 (5): 489-496.
Carvalho G, Rassi S, Bastos JM, Câmara SS. Asymptomatic coronary artery disease in chagasic patients with heart failure: prevalence and risk factors. Arq Bras Cardiol. 2011; 97 (5): 408-412.
Soares FA, Silveira TC. Accumulation of brown adipose tissue in patients with Chagas heart disease. Trans R Soc Trop Med Hyg. 1991; 85 (5): 605-607.
Long RG, Albuquerque RH, Prata A, Barnes AJ, Adrian TE, Christofides ND et al. Response of plasma pancreatic and gastrointestinal hormones and growth hormone to oral and intravenous glucose and insulin hypoglycaemia in Chagas disease. Gut. 1980; 21 (9): 772-777.
Rocha A, de Oliveira LC, Alves RS, Lopes ER. Pancreatic neuronal loss in chronic Chagas’ disease patients. Rev Soc Bras Med Trop. 1998; 31 (1): 43-49.
Saldanha JC, dos Santos VM, dos Reis MA, da Cunha DF, Antunes-Teixeira VP. Morphologic and morphometric evaluation of pancreatic islets in chronic Chagas’ disease. Rev Hosp Clin Fac Med Sao Paulo. 2001; 56 (5): 131-138.