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Los canales hipotálamicos K (((ATP) controlan la producción de glucosa hepática.

Alessandro Pocai1, Tony K T Lam, Roger Gutierrez-Juarez

  • 1Department of Medicine, Diabetes Research Center, Albert Einstein College of Medicine, Bronx, New York 10461, USA.

Nature
|April 23, 2005
PubMed
Resumen

La activación de los canales hipotalámicos K (((ATP) reduce la glucosa en sangre al inhibir la producción de glucosa en el hígado. Las interrupciones en esta vía cerebro-hígado contribuyen a la hiperglucemia diabética.

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Área de la Ciencia:

  • La neurociencia es la neurociencia.
  • Investigación Metabólica de Investigación.
  • Endocrinología Endocrinología.

Sus antecedentes:

  • La obesidad impulsa la prevalencia de la diabetes mellitus tipo 2 en todo el mundo.
  • La hiperglucemia en la diabetes está relacionada con el aumento de la gluconeogénesis hepática.
  • El hipotálamo medial integra las señales que regulan el equilibrio energético y la producción de glucosa hepática.

Objetivo del estudio:

  • Para investigar el papel de los canales hipotalámicos de potasio (K(ATP)) sensibles al ATP en el metabolismo de la glucosa.
  • Para determinar si la activación del canal K (((ATP) en el hipotálamo afecta a la gluconeogénesis hepática.
  • Explorar la contribución del circuito del sistema nervioso central y el hígado a la hiperglucemia diabética.

Principales métodos:

  • Activación de los canales K (((ATP) en el hipotálamo mediobasal.
  • Infusión de bloqueadores de los canales K (((ATP) en el hipotálamo mediobasal.
  • Resección quirúrgica de la rama hepática del nervio vago.
  • Análisis del metabolismo de la glucosa en ratones que carecen de la subunidad SUR1 de los canales K (ATP).

Principales resultados:

  • La activación del canal hipotálamo K (((ATP) redujo la glucosa en sangre al inhibir la gluconeogénesis hepática.
  • El bloqueo de los canales K (ATP) o la ruptura del nervio vago anulaban los efectos de la insulina central en la producción de glucosa hepática.
  • Los ratones que carecían de la subunidad SUR1 eran resistentes a los efectos inhibidores de la insulina en la gluconeogénesis.

Conclusiones:

  • Los canales hipotalámicos K (((ATP) normalmente restringen la gluconeogénesis hepática.
  • La disfunción en el circuito hígado-sistema nervioso central que involucra los canales K (ATP) contribuye a la hiperglucemia diabética.
  • Dirigirse a los canales hipotalámicos K (((ATP) puede ofrecer una nueva estrategia terapéutica para el manejo de la diabetes tipo 2.