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El aumento en el amiloide sérico a evocado por el colesterol dietético se asocia con un aumento de la aterosclerosis

Katherine E Lewis¹, Elizabeth A Kirk, Thomas O McDonald

¹Department of Medicine, University of Washington, Seattle, Wash 98195-6426, USA.

|July 28, 2004

Resumen

Las dietas altas en grasas aumentan el amiloide sérico A (SAA) y la aterosclerosis en ratones. Este estudio sugiere que la AAS promueve la aterosclerosis independientemente del colesterol, al mejorar la retención de lipoproteínas en los vasos sanguíneos.

Área de la Ciencia:

Investigaciones cardiovasculares en la investigación cardiovascular.
El metabolismo de los lípidos.
La patogénesis y la patogénesis de la aterosclerosis.

Sus antecedentes:

El nivel elevado de amiloide sérico A (SAA) está relacionado con el riesgo cardiovascular.
La grasa y el colesterol de la dieta pueden aumentar los niveles de AAS.
Los AAS pueden promover la aterogénesis al facilitar la unión lipoproteína-proteoglicano.

Objetivo del estudio:

Investigar si los aumentos de AAS inducidos por la dieta promueven la aterosclerosis independientemente del colesterol plasmático.
Explorar el papel directo de la AAS en el desarrollo de la aterosclerosis.

Principales métodos:

Los ratones hembra sin receptor de LDL fueron alimentados con dietas altas en grasas con o sin colesterol durante 10 semanas.
Se midieron los niveles plasmáticos de AAS y colesterol.
Se analizó la extensión de la aterosclerosis y la presencia de AAS en las lesiones.

Principales resultados:

Las dietas altas en grasas aumentaron los niveles plasmáticos de AAS.
El colesterol dietético elevó aún más la AAS sin aumentar el colesterol plasmático.
El aumento de los niveles de AAS se correlacionó con una mayor aterosclerosis.
La AAS se encontró en lesiones ateroscleróticas, lo que sugiere un papel directo.

Conclusiones:

El colesterol en la dieta aumenta la AAS y la aterosclerosis independientemente de las lipoproteínas plasmáticas.
La AAS puede promover directamente la aterosclerosis mediante la mediación de la retención de HDL enriquecido con AAS a los proteoglicanos vasculares.

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