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El coactivador del CREB TORC2 es un regulador clave del metabolismo de la glucosa en ayunas
Seung-Hoi Koo1, Lawrence Flechner, Ling Qi
1Peptide Biology Laboratories, Salk Institute for Biological Studies, 10010 N Torrey Pines Rd, La Jolla, California 92037-1002, USA.
Nature
|September 9, 2005
Resumen
Las señales hormonales y energéticas convergen en TORC2 (transductor de la actividad regulada de CREB 2) para controlar la producción de glucosa en el hígado. La activación de AMPK inhibe la gluconeogénesis al bloquear la entrada nuclear de TORC2, ofreciendo terapias potenciales para la diabetes tipo 2.
Área de la Ciencia:
- Regulación del metabolismo.
- La señalización hormonal.
- La detección de energía celular.
Sus antecedentes:
- La homeostasis de la glucosa depende de las hormonas sistémicas (insulina, glucagón) y del estado energético celular.
- El glucagón promueve la producción de glucosa hepática a través de la activación de CREB (proteína de unión del elemento de respuesta CAMP).
- La proteína quinasa activada por AMP (AMPK) inhibe la gluconeogénesis hepática bajo niveles bajos de ATP, pero el mecanismo no está claro.
Objetivo del estudio:
- Para dilucidar el mecanismo por el cual AMPK inhibe la gluconeogénesis hepática.
- Identificar el punto de convergencia de las vías hormonales y de detección de energía en la regulación de la glucosa.
- Para investigar el papel de TORC2 (transductor de la actividad regulada CREB 2) en la modulación de la salida de glucosa.
Principales métodos:
- Investigó la interacción entre la señalización de AMPK, TORC2 y CREB.
- Utilizó técnicas de biología celular y molecular para rastrear la localización y la actividad de TORC2.
- Se examinó el impacto de la activación de AMPK en la fosforilación de TORC2 y la translocación nuclear.
Principales resultados:
- Las vías hormonales y de detección de energía convergen en el coactivador TORC2.2.
- El TORC2 se desplaza entre el citoplasma y el núcleo, regulando la transcripción dependiente del CREB de los genes gluconeogénicos.
- La activación de AMPK promueve la fosforilación de TORC2, previniendo su acumulación nuclear e inhibiendo la gluconeogénesis.
Conclusiones:
- TORC2 actúa como un integrador clave de las señales hormonales y energéticas en la producción de glucosa hepática.
- La inhibición mediada por AMPK de la importación nuclear de TORC2 es un mecanismo crítico para suprimir la gluconeogénesis.
- La focalización de la fosforilación TORC2 puede representar una estrategia terapéutica para el manejo de la hiperglucemia en ayunas en la diabetes tipo 2.
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