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El alelo de inserción del polimorfismo I/D del gen ACE. ¿Un gen candidato para la resistencia a la insulina?

A Panahloo¹, C Andrès, V Mohamed-Ali

¹Department of Medicine, University College London Medical School, Whittington Hospital, England.

|December 15, 1995

Resumen

El genotipo de deleción de la enzima convertidora de angiotensina (ACE) (DD) está relacionado con un mayor riesgo de enfermedad coronaria (CHD). Este estudio no encontró ninguna asociación con la resistencia a la insulina, pero reveló un aumento de la sensibilidad a la insulina en sujetos NIDDM con el genotipo DD.

Área de la Ciencia:

Genética La genética.
Enfermedades cardiovasculares Enfermedades cardiovasculares Enfermedades cardiovasculares Enfermedades cardiovasculares Enfermedades cardiovasculares Enfermedades cardiovasculares Enfermedades cardiovasculares Enfermedades cardiovasculares
El síndrome metabólico.

Sus antecedentes:

El polimorfismo de inserción/eliminación (ID) de la enzima convertidora de angiotensina (ACE) está relacionado con la enfermedad coronaria (CHD), pero el mecanismo subyacente sigue sin estar claro.
Este estudio investigó la posible asociación entre el alelo de deleción del gen ACE y la resistencia a la insulina.

Objetivo del estudio:

Para probar la hipótesis de que el alelo de deleción del gen ACE está asociado con la resistencia a la insulina.
Explorar la relación entre el genotipo ACE y los componentes del síndrome de resistencia a la insulina.

Principales métodos:

Se realizó genotipización para el polimorfismo de inserción/eliminación (ID) de la ECA.
La sensibilidad a la insulina, los niveles de insulina y el des 31,32 de proinsulina se midieron en 103 sujetos blancos diabéticos no dependientes de insulina (NIDDM) y 533 no diabéticos.
El análisis incluyó cálculos de ANOVA y HOMA %.

Principales resultados:

Los sujetos NIDDM con el genotipo DD mostraron niveles de insulina específica significativamente más bajos en comparación con los genotipos ID y II.
Los sujetos no tratados con insulina con el genotipo DD exhibieron una mayor sensibilidad a la insulina y niveles más bajos de proinsulina.
No se observaron diferencias significativas en la prevalencia de ECC, la presión arterial, los lípidos séricos o la actividad PAI-1 entre los genotipos ACE en los grupos diabéticos o no diabéticos.

Conclusiones:

El aumento del riesgo cardiovascular asociado con el genotipo ACE DD no está mediado por la resistencia a la insulina o las anomalías de la fibrinólisis.
Se observó un aumento de la sensibilidad a la insulina en sujetos NIDDM portadores del genotipo ACE DD.

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