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Las neuronas AgRP controlan la sensibilidad sistémica a la insulina a través de la expresión de miostatina en el

Sophie M Steculorum¹, Johan Ruud¹, Ismene Karakasilioti¹

¹Department of Neuronal Control of Metabolism, Max Planck Institute for Metabolism Research, Gleueler Strasse 50, 50931 Cologne, Germany; Center for Endocrinology, Diabetes and Preventive Medicine (CEDP), University Hospital Cologne, Kerpener Strasse 26, 50924 Cologne, Germany; Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases (CECAD) and Center for Molecular Medicine Cologne (CMMC), University of Cologne, Joseph-Stelzmann-Strasse 26, 50931 Cologne, Germany.

|March 26, 2016

Resumen

La activación de las neuronas peptídicas relacionadas con Agouti (AgRP) impulsa la alimentación y la resistencia a la insulina mediante la reprogramación de la grasa marrón. La miostatina mejora la sensibilidad a la insulina, revelando un vínculo entre el hambre y el control de la glucosa.

Área de la Ciencia:

La neurociencia
El metabolismo
Endocrinología

Sus antecedentes:

Las neuronas peptídicas relacionadas con Agouti (AgRP) regulan el comportamiento de alimentación.
La actividad crónica de las neuronas AgRP influye en la homeostasis de la glucosa.
No se comprende completamente el impacto de la activación aguda de las neuronas AgRP en la sensibilidad a la insulina.

Objetivo del estudio:

Investigar los efectos agudos de la activación de las neuronas AgRP en la resistencia a la insulina.
Identificar los mecanismos por los que las neuronas AgRP influyen en la absorción de glucosa en el tejido adiposo marrón (TAB).
Para explorar el papel de la miostatina en la resistencia a la insulina mediada por las neuronas AgRP.

Principales métodos:

La activación optogenética de las neuronas AgRP en ratones.
Medición de la absorción de glucosa estimulada por insulina en las MTD.
Análisis de la expresión génica de las MTD, centrado en marcadores miogénicos como la miostatina.
Mapeo de circuitos optogenéticos para delinear proyecciones específicas de neuronas AgRP.

Principales resultados:

La activación aguda de las neuronas AgRP induce la resistencia a la insulina al deteriorar la absorción de glucosa en las MTD.
La activación de las neuronas AgRP aumenta la expresión de miostatina en las MTD, promoviendo una firma miogénica.
La interferencia con la actividad de la miostatina mejora la resistencia a la insulina inducida por las neuronas AgRP.
Las proyecciones de neuronas AgRP diferenciadas controlan la alimentación y la sensibilidad a la insulina a través de las vías de miostatina de las MTD.

Conclusiones:

Las neuronas AgRP coordinan agudamente el comportamiento de alimentación con la resistencia a la insulina.
Las neuronas AgRP inducen la resistencia a la insulina promoviendo la expresión génica relacionada con el músculo en las MTD.
Este estudio revela un nuevo mecanismo que vincula los circuitos del hambre con la regulación metabólica a través de la reprogramación de las MTD.

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