INSULINORRESISTENCIA Y OBESIDAD PDF

Palabras clave: Adiponectina, Obesidad, Enfermedades cardiovasculares, Adipocinas. Abstract: Obesity is closely associated to the metabolic syndrome, hypertension, atherosclerosis, and heart disease. Adipose tissue works as an endocrine organ by secreting multiple immune modulatory proteins known as adipokines, which can act directly on nearby or remote organs. Adipokines seem to be the link between obesity and cardiovascular disease.

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Insulinorresistencia e hiperinsulinemia como factores de riesgo para enfermedad cardiovascular. Facultad de Medicina. La Universidad del Zulia. Maracaibo-Venezuela e-Mail: vbermudez hotmail.

Palabras clave: insulinoresistencia, hiperinsulinemia, insulina, enfermedad cardiovascular. Insulin resistance is defined as a metabolic state in which insulin peripheral effects are diminished. Several years ago several authors are agree with the fact that insulin resistance and hiperinsulinemia are involved in hypertension, obesity and diabetes. Equally, hyperinsulinemia is related with a plasmatic lipidic pattern characterized by a decrease in HDL cholesterol and increases in triglyceride and VLDL levels that in turn conduces to atherosclerosis development.

In this sense, myocardial ischemia has been related with these conditions in both, genesis and further evolution because accelerated atherosclerosis and myocyte survival reduction by angiogenesis blockade at insulin-signalling level. Hyperinsulinemia is related with myocardial hypertrophy.

One hypothesis that has been designed to explain this association is that insulin may directly increase blood pressure and therefore left ventricular work. In support of this, insulin has been shown to activate the sympathetic nervous system in patients with essential hypertension. Finally, impaired insulin sensitivity is highly prevalent among non-diabetic patients with a recent TIA or non-disabling ischemic stroke. This finding has important therapeutic implications if treatment to improve insulin sensitivity is shown to reduce risk for subsequent stroke and heart disease.

Key words: insulin resistance, hiperinsulinemia, insulin, cardiovascular disease. Para ello utiliza los residuos de tirosina ya fosforilados como sitios de anclaje. Bases moleculares y celulares de la insulinorresistencia. Las endotelinas son potentes vasoconstrictoras de 21 aa codificadas por 3 genes en diferentes tejidos del cuerpo.

Endotelina 1 ET-1 es la principal generada por el endotelio, actuando de forma paracrina y autocrina sobre los receptores ET A y ET B y sus efectos dependen del lecho vascular donde se encuentren. Insulinorresistencia, hiperinsulinemia y arritmias. Insulinorresistencia, hiperinsulinemia y aterosclerosis. El GLUT1 es el responsable del transporte basal del la glucosa en los cardiomiocitos, para luego ser traslocados velozmente al sarcolema en respuesta a la isquemia. Se ha relacionado la IR e hiperinsulinemia como factores asociados a la hipertrofia ventricular.

Servicios Personalizados Articulo. Similares en SciELO. Palabras clave: insulinoresistencia, hiperinsulinemia, insulina, enfermedad cardiovascular Abstract Insulin resistance is defined as a metabolic state in which insulin peripheral effects are diminished.

Endotelina-1 Las endotelinas son potentes vasoconstrictoras de 21 aa codificadas por 3 genes en diferentes tejidos del cuerpo. Referencias 1. Williams, B. Lancet ; Himsworth, H. Luo R, et al. Science ; White, M. Rescent Prog Horm Res ; Cheatham B, Kahn C.

Endocr Rev ; Le Roith, D, Zick Y. Diabetes Care ; Pearson G, et al. Endocrin Rev ;22 2 Kusari A, et al. Mol Endocrinol ;11 10 Sadagurski M, Weingarten G. J Biol Chem ; Mol Biol Cell ;9 11 Wajchenberg, B L. Endocrine Reviews ;21 6 Hill, J O. Science ; : Bjorntorp, P. Acta Med Scand Suppl. Derpress, J P. Nutrition ; Koyama, K. Physiol Endrocrinol Metab ;EE Kahn B B. J Clin Invest ; 4 Koska J, Ortega E.

Roden M, et al. J Clin Invest ; Griffin M, et al. Diabetes ; Shulman, G. J Clin Invest ; 2 Stein D, et al. Hotamisligil G, Spiegelman B. Science ; Qi C, Pekala P. M ; Kieffer TJ. Am J Physiol Endocrinol Metab.

Emilsson V, et al. Endocrinology ; 10 Hebert L, et al. J Clin Invest ;98 4 Endocrinology ; 6 Vossller K, et al. Reaven G, Hoffman B. Lancet ; Saad M. Reaven GM, Chang H. Am J Hypertens. Hofman P. Hypertension ;34 part 2 Margolis RU, Altszuler N. Am J Physiol. J Clin Invest. Am J Hypertens ; Campbell W, et al. Circulation Research ; Capdevila J. Lipid Res. Miller A, et al. J Cardiovasc Pharmacol ; Sowers J.

Hypertension ; Sowers JR. Chambers et al.

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