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Lecitina funcional: la colesterol aciltransferasa no es necesaria para una eficiente atheroprotección en humanos
Laura Calabresi1, Damiano Baldassarre, Samuela Castelnuovo
1Center E. Grossi Paoletti, Department of Pharmacological Sciences, Università degli Studi di Milano, 20133 Milano, Italy.
Circulation
|August 19, 2009
Resumen
Lecitina: la deficiencia de colesterol aciltransferasa (LCAT), a pesar de causar lipoproteínas de baja y alta densidad, no aumenta el riesgo cardiovascular. Este estudio no encontró una mayor aterosclerosis preclínica en portadores de deficiencia de LCAT, lo que desafía la LCAT.
Área de la Ciencia:
- Genética La genética.
- Trastornos metabólicos Los trastornos metabólicos son trastornos metabólicos que se producen en el cuerpo.
- Enfermedades cardiovasculares Enfermedades cardiovasculares Enfermedades cardiovasculares Enfermedades cardiovasculares Enfermedades cardiovasculares Enfermedades cardiovasculares Enfermedades cardiovasculares Enfermedades cardiovasculares
Sus antecedentes:
- Lecitina: la deficiencia de colesterol aciltransferasa (LCAT), causada por mutaciones en el gen LCAT, resulta en hipoalfalipoproteinemia.
- Existen dos formas: deficiencia familiar de LCAT (ausencia completa de la enzima) y enfermedad de los ojos de los peces (defecto parcial de la enzima).
- La deficiencia de LCAT teóricamente aumenta el riesgo cardiovascular debido a la lipoproteína de baja alta densidad (HDL) y la alteración del transporte inverso del colesterol.
Objetivo del estudio:
- Para evaluar la aterosclerosis preclínica en individuos con mutaciones en el gen LCAT.
- Investigar la relación entre la deficiencia de LCAT y los factores de riesgo cardiovascular.
- Para determinar si la actividad de LCAT es esencial para la atheroprotección.
Principales métodos:
- El espesor íntima-medio de la carótida (IMT) se midió en 40 portadores de mutaciones LCAT de 13 familias italianas.
- Para la comparación, se incluyó un grupo de control de 80 individuos sanos.
- Se analizó el efecto de la dosis de genes del genotipo LCAT en el IMT carotídeo.
Principales resultados:
- El IMT carotídeo fue significativamente menor en los portadores de la mutación LCAT en comparación con los controles.
- Se observó un efecto dependiente de la dosis de los genes del genotipo LCAT mutado, reduciendo el IMT carotídeo.
- No se encontró ninguna diferencia significativa en el IMT carotídeo entre los portadores de deficiencia familiar de LCAT y la enfermedad del ojo de pez.
Conclusiones:
- La baja actividad LCAT determinada genéticamente no se asocia con un aumento de la aterosclerosis preclínica.
- Este hallazgo desafía el papel establecido de LCAT en la ateroprotección.
- El aumento de la actividad LCAT puede no ser una estrategia viable para reducir el riesgo cardiovascular.
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