CONTROVERSIAS ACERCA DE LA INTERACCION EXACTA ENTRE EL SISTEMA SIMPATICO Y LA RESISTENCIA A LA INSULINA EN LA OBESIDAD Y LA HIPERTENSION
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CONTROVERSIAS ACERCA DE LA INTERACCION EXACTA ENTRE EL SISTEMA SIMPATICO Y LA RESISTENCIA A LA INSULINA EN LA OBESIDAD Y LA HIPERTENSION

(especial para SIIC © Derechos reservados)
El aumento de la actividad simpática y de la resistencia a la insulina son hallazgos bien establecidos en obesidad e hipertensión.
Autor:
Kazuko Masuo
Columnista Experto de SIIC

Institución:
Baker Heart Research Institute


Artículos publicados por Kazuko Masuo
Coautores
Gavin W. Lambert* Murray D. Esler* 
Baker Heart Research Institute, Melbourne, Australia*
Recepción del artículo
2 de Abril, 2008
Aprobación
8 de Mayo, 2008
Primera edición
24 de Julio, 2009
Segunda edición, ampliada y corregida
7 de Junio, 2021

Resumen
La obesidad, la hipertensión y la hipertensión relacionada con la obesidad son problemas crecientes en salud pública. El aumento de la actividad simpática y de la resistencia a la insulina son hallazgos bien establecidos en obesidad e hipertensión. Sin embargo, existe información controvertida sobre la forma de interacción precisa entre la actividad simpática y la resistencia a la insulina en obesidad e hipertensión. En otras palabras, no se ha aclarado cuál es el primus movens en obesidad e hipertensión, en el aumento de la actividad simpática o de la resistencia a la insulina. La obesidad y la hipertensión tienen un fuerte determinante genético. La reducción en el gasto de energía y de la tasa metabólica en reposo predice un aumento de peso; el sistema nervioso simpático participa en la regulación del balance energético a través de la termogénesis. El efecto termogénico de las catecolaminas en la obesidad está mediado en los humanos a través de los receptores adrenérgicos β2 y β3. Además los receptores β2 influyen de manera importante sobre la reactividad vascular. Los polimorfismos genéticos del gen receptor adrenérgico β mostraron que alteran la función de los receptores adrenérgicos subtipos β2 y β3 y modifican de esa manera la actividad del sistema simpático (catecolaminas). Los polimorfismos genéticos del gen receptor adrenérgico β, especialmente Arg16Gly y Gln27Glu entre los polimorfismos de los receptores adrenérgicos β2 y del Trp64Arg del receptor adrenérgico β3, están asociados con obesidad, hipertensión y resistencia a la insulina. El propósito de este artículo es revisar los conocimientos actuales sobre la relación entre la actividad del sistema simpático, la resistencia a la insulina, los polimorfismos de los receptores adrenérgicos beta, obesidad, e hipertensión para comprender mejor los papeles precisos de la actividad simpática y la resistencia a la insulina en la obesidad y en la hipertensión.

Palabras clave
actividad del sistema nervioso simpático, resistencia a la insulina, polimorfismo de los adrenorreceptores beta 2, polimorfismo de los adrenorreceptores beta 3, obesidad, hipertensión, hipertensión relacionada con obesidad


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Abstract
Obesity, hypertension, and obesity-related hypertension are rapidly growing public health problems. Heightened sympathetic nerve activity and insulin resistance are well-established observations in obesity and hypertension. However, conflicting information regarding the precise interactions between sympathetic nerve activity and insulin resistance in obesity and hypertension remain. In other words, the argument which is a primary mover in obesity and hypertension, of heightened sympathetic nerve activity or insulin resistance, has not been clarified. Obesity and hypertension have a strong genetic determinant. Reduced energy expenditure and resting metabolic rate are predictive of weight gain, and the sympathetic nervous system participates in regulating energy balance through thermogenesis. The thermogenic effects of catecholamines in obesity have been mainly mediated via the 2 and 3-adrenergic receptors in humans. Further, ß-adrenoceptors importantly influence vascular reactivity. Genetic polymorphisms of the -adrenoceptor gene have been shown to alter the function of ß2- and ß3-adrenoceptor subtype and thus to modify the response to sympathetic nerve activity (catecholamines). Genetic polymorphisms of the ß-adrenoceptor gene, especially Arg16Gly and Gln27Glu among the 2-adrenoceptor polymorphisms and Trp64Arg of the 3-adrenoceptor, are associated with obesity, hypertension and insulin resistance. The purpose of this article is to provide the current findings on the relationships between sympathetic nerve activity, insulin resistance, ß-adrenoceptor polymorphisms, obesity, and hypertension to further understand the precise roles of sympathetic nerve activity and insulin resistance in obesity and hypertension.

Key words
sympathetic nerve activity, insulin resistance, ß2-adrenoceptor polymorphisms, ß3-adrenoceptor polymorphisms, obesity, hypertension, obesity-related hypertension


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Clasificación en siicsalud
Artículos originales > Expertos del Mundo >
página   www.siicsalud.com/des/expertocompleto.php/

Especialidades
Principal: Cardiología
Relacionadas: Atención Primaria, Bioquímica, Diabetología, Diagnóstico por Laboratorio, Endocrinología y Metabolismo, Geriatría, Medicina Familiar, Medicina Interna, Neurología, Nutrición



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Kazuko Masuo, Baker Heart Research Institute Human Neurotransmitter Laboratory, 8008, PO Box 6492 St Kilda Road Central, Melbourne, Australia
Bibliografía del artículo

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