2016, Número 2
<< Anterior Siguiente >>
Rev Cubana Invest Bioméd 2016; 35 (2)
Mecanismos moleculares de la obesidad y el rol de las adipocinas en las enfermedades metabólicas
Irecta NCA, Álvarez GGC
Idioma: Español
Referencias bibliográficas: 40
Paginas: 174-183
Archivo PDF: 526.76 Kb.
RESUMEN
La obesidad es un problema de salud pública a nivel mundial, se estima que el 52 %
de los adultos y el 30 % de los niños sufren exceso de peso. Los mecanismos
moleculares implicados en la obesidad permiten la comprensión de las enfermedades
asociadas a ella como la hipertensión, enfermedades cardiometabólicas, eventos
cerebrovasculares y resistencia a la insulina. Por una parte los eventos moleculares
afectan las señales producidas por la insulina permitiendo su resistencia, por otra
parte se induce un estado inflamatorio sostenido característico de las personas
obesas, que están implicados en la formación de placas ateromatosas, estimulación de
un estado protrombótico sostenido y aparición de eventos isquémicos. En estas
enfermedades el estudio de las adipocinas como leptina adiponectina, factor de
necrosis tumoral alfa, proteína c Reactiva, permite conocer el vínculo de la obesidad
con las enfermedades crónicas además de ser un blanco de estudio activo para su
utilidad diagnóstica.
REFERENCIAS (EN ESTE ARTÍCULO)
Barrera-Cruz A, Rodríguez-González A, Molina-Ayala M. Escenario actual de la obesidad en México. Rev Med Inst Mex Seguro Soc. 2013;51:292-9.
Lau DC, Dhillon B, Yan H, Szmitko PE, Verma S. Adipokines: molecular links between obesity and atheroslcerosis. American Journal of Physiology-Heart and Circulatory Physiology. 2005;288:H2031-H41.
Kopelman PG. Obesity as a medical problem. Nature. 2000;404:635-43.
Mohamed-Ali V, Pinkney J, Coppack S. Adipose tissue as an endocrine and paracrine organ. International journal of obesity. 1998;22:1145-58.
Weisberg SP, McCann D, Desai M, Rosenbaum M, Leibel RL, Ferrante Jr AW, et al. Obesity is associated with macrophage accumulation in adipose tissue. Journal of clinical investigation. 2003;112:1796.
Meissburger B. Molecular mechanisms of adipogenesis in obesity and the metabolic syndrome: Diss., Eidgenössische Technische Hochschule ETH Zürich, Nr; 2010.
Misra KB, Kim KC, Cho S, Low MG, Bensadoun A. Purification and characterization of adipocyte heparan sulfate proteoglycans with affinity for lipoprotein lipase. Journal of Biological Chemistry. 1994;269:23838-44.
Ray R, Shah Axam. NADPH oxidase and endothelial cell function. Clinical Science. 2005;109:217-26.
Pilz S, März W. Free fatty acids as a cardiovascular risk factor. Clinical Chemistry and Laboratory Medicine. 2008;46:429-34.
Noronha BT, Li J-M, Wheatcroft SB, Shah AM, Kearney MT. Inducible nitric oxide synthase has divergent effects on vascular and metabolic function in obesity. Diabetes. 2005;54:1082-9.
Shi Y, Burn P. Lipid metabolic enzymes: emerging drug targets for the treatment of obesity. Nature Reviews Drug Discovery. 2004;3:695-710.
Lumeng CN, Bodzin JL, Saltiel AR. Obesity induces a phenotypic switch in adipose tissue macrophage polarization. Journal of Clinical Investigation. 2007;117:175.
Nakamura K, Fuster JJ, Walsh K. Adipokines: a link between obesity and cardiovascular disease. Journal of cardiology. 2014;63:250-9.
Ouchi N, Kihara S, Funahashi T, Matsuzawa Y, Walsh K. Obesity, adiponectin and vascular inflammatory disease. Current opinion in lipidology. 2003;14:561-6.
Berg AH, Scherer PE. Adipose tissue, inflammation, and cardiovascular disease. Circulation research. 2005;96:939-49.
Ouchi N, Higuchi A, Ohashi K, Oshima Y, Gokce N, Shibata R, et al. Sfrp5 is an anti-inflammatory adipokine that modulates metabolic dysfunction in obesity. Science. 2010;329:454-7.
Simón E, Del Barrio A. Leptina y obesidad. Anales del sistema sanitario de Navarra; 2002. p. 53-64.
Ghizzoni L, Mastorakos G. Interactions of leptin, GH, and cortisol in normal children. Annals of the New York Academy of Sciences. 2003;997:56-63.
Marx J. Cellular warriors at the battle of the bulge. Science. 2003;299:846.
Uysal KT, Wiesbrock SM, Marino MW, Hotamisligil GS. Protection from obesityinduced insulin resistance in mice lacking TNF-α function. Nature. 1997;389:610-4.
Hotamisligil GS, Budavari A, Murray D, Spiegelman BM. Reduced tyrosine kinase activity of the insulin receptor in obesity-diabetes. Central role of tumor necrosis factor-alpha. Journal of Clinical Investigation. 1994;94:1543.
Kleinbongard P, Heusch G, Schulz R. TNFα in atherosclerosis, myocardial ischemia/reperfusion and heart failure. Pharmacology & therapeutics. 2010;127:295-314.
Bruunsgaard H, Skinhøj P, Pedersen AN, Schroll M, Pedersen B. Ageing, tumour necrosis factor ‐alpha (TNF‐α) and atherosclerosis. Clinical & Experimental Immunology. 2000;121:255-60.
Ohta H, Wada H, Niwa T, Kirii H, Iwamoto N, Fujii H, et al. Disruption of tumor necrosis factor-alpha gene diminishes the development of atherosclerosis in ApoEdeficient mice. Atherosclerosis. 2005;180:11-7.
Xiao N, Yin M, Zhang L, Qu X, Du H, Sun X, et al. Tumor necrosis factor-alpha deficiency retards early fatty-streak lesion by influencing the expression of inflammatory factors in apoE-null mice. Molecular genetics and metabolism. 2009;96:239-44.
Slowik MR, De Luca LG, Fiers W, Pober JS. Tumor necrosis factor activates human endothelial cells through the p55 tumor necrosis factor receptor but the p75 receptor contributes to activation at low tumor necrosis factor concentration. The American journal of pathology. 1993;143:1724.
Boesten LS, Zadelaar ASM, van Nieuwkoop A, Gijbels MJ, de Winther MP, Havekes LM, et al. Tumor necrosis factor-α promotes atherosclerotic lesion progression in APOE* 3-leiden transgenic mice. Cardiovascular research. 2005;66:179-85.
Kadokami T, McTiernan CF, Kubota T, Frye CS, Feldman AM. Sex-related survival differences in murine cardiomyopathy are associated with differences in TNF-receptor expression. Journal of Clinical Investigation. 2000;106:589.
Wajant H, Pfizenmaier K, Scheurich P. Tumor necrosis factor signaling. Cell Death & Differentiation. 2003;10:45-65.
Hu E, Liang P, Spiegelman BM. AdipoQ is a novel adipose-specific gene dysregulated in obesity. Journal of Biological Chemistry. 1996;271:10697-703.
Maeda K, Okubo K, Shimomura I, Funahashi T, Matsuzawa Y, Matsubara K. cDNA cloning and expression of a novel adipose specific collagen-like factor, apM1 (adipose most abundant gene transcript 1). Biochemical and biophysical research communications. 1996;221:286-9.
Scherer PE, Williams S, Fogliano M, Baldini G, Lodish HF. A novel serum protein similar to C1q, produced exclusively in adipocytes. The Journal of biological chemistry. 1995;270:26746-9.
Arita Y. Reprint of “Paradoxical Decrease of an Adipose-Specific Protein, Adiponectin, in Obesity”. Biochemical and biophysical research communications. 2012;425:560-4.
Tomas E, Tsao T-S, Saha AK, Murrey HE, Cheng Zhang C, Itani SI, et al. Enhanced muscle fat oxidation and glucose transport by ACRP30 globular domain: Acetyl–CoA carboxylase inhibition and AMP-activated protein kinase activation. Proceedings of the National Academy of Sciences. 2002;99:16309-13.
Yamauchi T, Kamon J, Minokoshi Ya, Ito Y, Waki H, Uchida S, et al. Adiponectin stimulates glucose utilization and fatty-acid oxidation by activating AMP-activated protein kinase. Nature medicine. 2002;8:1288-95.
Sattar N, Wannamethee G, Sarwar N, Tchernova J, Cherry L, Wallace AM, et al. Adiponectin and Coronary Heart Disease A Prospective Study and Meta-Analysis. Circulation. 2006;114:623-9.
Iwashima Y, Katsuya T, Ishikawa K, Ouchi N, Ohishi M, Sugimoto K, et al. Hypoadiponectinemia is an independent risk factor for hypertension. Hypertension. 2004;43:1318-23.
Hong SJ, Park CG, Seo HS, Oh DJ, Ro YM. Associations among plasma adiponectin, hypertension, left ventricular diastolic function and left ventricular mass index. Blood pressure. 2004;13:236-42.
Ouchi N, Kihara S, Arita Y, Maeda K, Kuriyama H, Okamoto Y, et al. Novel modulator for endothelial adhesion molecules adipocyte-derived plasma protein adiponectin. Circulation. 1999;100:2473-6.
Ouchi N, Kihara S, Arita Y, Okamoto Y, Maeda K, Kuriyama H, et al. Adiponectin, an adipocyte-derived plasma protein, inhibits endothelial NF-kappaB signaling through a cAMP-dependent pathway. Circulation. 2000;102:1296-301.