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El receptor nuclear LXR es un sensor de glucosa
Nico Mitro1, Puiying A Mak, Leo Vargas
1Genomics Institute of the Novartis Research Foundation, 10675 John Hopkins Drive, San Diego, California 92121, USA.
Nature
|December 26, 2006
Resumen
La glucosa activa directamente el receptor X del hígado (LXR), un regulador clave del metabolismo de los lípidos. Este hallazgo revela un nuevo mecanismo de cómo la glucosa controla su propio destino metabólico en el hígado.
Área de la Ciencia:
- Regulación del metabolismo.
- Biología molecular La biología molecular.
- Hepatología Hepatología.
Sus antecedentes:
- El hígado juega un papel crucial en el mantenimiento de la homeostasis de la glucosa a través de la producción y el consumo.
- La insulina y el ChREBP son reguladores conocidos del metabolismo hepático de la glucosa y la lipogénesis.
- Los mecanismos precisos por los cuales la glucosa influye en su propio destino metabólico aún están bajo investigación.
Objetivo del estudio:
- Investigar un nuevo mecanismo por el cual la glucosa regula su propio destino metabólico en el hígado.
- Para determinar si la glucosa interactúa directamente con y modula la actividad del receptor X del hígado (LXR).
Principales métodos:
- Ensayos bioquímicos para probar la unión directa y la activación de LXR-alfa y LXR-beta por glucosa y glucosa-6-fosfato.
- Análisis de la expresión génica de los genes diana LXR en respuesta a la glucosa.
- Estudios in vivo en ratones para evaluar el impacto de una dieta de glucosa en los genes de la homeostasis del colesterol.
Principales resultados:
- d-Glucosa y d-glucosa-6-fosfato fueron identificados como agonistas directos tanto de LXR-alfa como de LXR-beta.
- La glucosa activa la LXR a concentraciones fisiológicas en el hígado, induciendo la expresión génica objetivo de manera similar a los oxisteroles.
- La expresión de los genes de homeostasis del colesterol dependientes de la LXR fue regulada al alza en ratones alimentados con glucosa, confirmando la glucosa como un ligando endógeno de la LXR.
Conclusiones:
- El receptor X hepático (LXR) actúa como un interruptor de transcripción que integra el metabolismo hepático de la glucosa y la síntesis de ácidos grasos.
- La glucosa estimula directamente la LXR, proporcionando un nuevo vínculo molecular entre la disponibilidad de glucosa y el metabolismo de los lípidos.
- Este estudio descubre una vía previamente no reconocida para la regulación de la glucosa de la síntesis de lípidos hepáticos.
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