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Un circuito de retroalimentación conservado de SREBP-1/fosfatidilcolina regula la lipogénesis en los metazoanos

Amy K Walker¹, René L Jacobs, Jennifer L Watts

¹Massachusetts General Hospital Cancer Center, Building 149, 13th Street, Charlestown, MA 02129, USA. amy_walker@mac.com

|November 1, 2011

Resumen

Las proteínas de unión de los elementos reguladores de esteroles (SREBPs) controlan el metabolismo de los lípidos. Los nuevos hallazgos revelan que la actividad de SREBP-1 está regulada por los niveles de fosfatidilcolina (PC), que vinculan la síntesis de lípidos a los trastornos metabólicos.

Área de la Ciencia:

Biología Molecular Biología Molecular
La bioquímica metabólica es una bioquímica metabólica.
Biología celular Biología celular.

Sus antecedentes:

Las proteínas de unión de los elementos reguladores de esteroles (SREBPs) son cruciales para la homeostasis de los lípidos.
La actividad desregulada de SREBP está implicada en el síndrome metabólico, incluida la obesidad y la enfermedad del hígado graso.

Objetivo del estudio:

Para investigar el circuito regulador controlado por SREBP-1.
Para aclarar el papel del ciclo de un carbono y la síntesis de fosfatidilcolina (PC) en la regulación de SREBP-1.

Principales métodos:

Estudios en C. elegans, hígado de ratón y células humanas.
Análisis de la expresión génica relacionada con el ciclo de un carbono.
Evaluación de la actividad de SREBP-1 y la acumulación de gotas de lípidos.

Principales resultados:

SREBP-1 controla los genes en el ciclo de un carbono, produciendo S-adenosilmetionina (SAMe).
La inhibición de la síntesis de SAMe o PC condujo a un aumento de la transcripción de SREBP-1 y la acumulación de lípidos.
La maduración nuclear del SREBP-1 está regulada por los niveles de PC, lo que sugiere un mecanismo de retroalimentación.

Conclusiones:

Un circuito regulador conservado enlaza el ciclo de un carbono y la síntesis de PC con la actividad de SREBP-1.
La producción limitada de SAMe o PC puede activar SREBP-1, lo que contribuye a los trastornos metabólicos.
Esto proporciona nuevos conocimientos sobre la base molecular de las enfermedades metabólicas.

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