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El glucagón estimula la gluconeogénesis por medio de la lipólisis hepática mediada por INSP3R1
Rachel J Perry1,2, Dongyan Zhang1, Mateus T Guerra1
1Department of Internal Medicine, Yale School of Medicine, New Haven, CT, USA.
Nature
|March 6, 2020
Resumen
El glucagón estimula la quema de grasa y la producción de glucosa en el hígado a través de INSP3R1. Dirigirse a este receptor puede revertir el hígado graso y la diabetes tipo 2.
Área de la Ciencia:
- Enfermedades metabólicas
- Hepatología
- Endocrinología
Sus antecedentes:
- La reducción de la relación insulina/ glucagón afecta el metabolismo hepático de la glucosa en la diabetes tipo 2.
- Los mecanismos de efecto del glucagón sobre la producción hepática de glucosa y la oxidación mitocondrial no están claros.
Objetivo del estudio:
- Aclarar los mecanismos por los que el glucagón influye en la producción hepática de glucosa y la oxidación mitocondrial.
- Investigar el papel del receptor de trifosfato de inositol 1 (INSP3R1) en la mediación de los efectos hepáticos del glucagón.
- Evaluar el potencial terapéutico de dirigirse a INSP3R1 para la enfermedad hepática grasa no alcohólica y la diabetes tipo 2.
Principales métodos:
- Se estudiaron los efectos del glucagón en la actividad de la lipasa triglicérida hepática, la lipólisis intrahepática, el contenido de acetil-CoA y el flujo de la carboxilasa piruvato en roedores.
- Se examinó la oxidación de la grasa mitocondrial en respuesta al glucagón.
- Se utilizaron ratones con knockout INSP3R1 (Itpr1) para evaluar la necesidad de INSP3R1 en la mediación de los efectos del glucagón.
- Se administró tratamiento crónico con glucagón a ratones y ratas obesos inducidos por la dieta.
Principales resultados:
- El glucagón estimula la gluconeogénesis hepática y la oxidación de la grasa mitocondrial mediante la activación de INSP3R1.
- El tratamiento crónico con glucagón en roedores revirtió la esteatosis hepática inducida por la dieta y la resistencia a la insulina.
- Estos efectos beneficiosos fueron abolidos en ratones con knockout INSP3R1, confirmando el papel crítico del receptor.
Conclusiones:
- La señalización de glucagón a través de INSP3R1 mejora la oxidación de la grasa hepática y la gluconeogénesis.
- La activación de INSP3R1 por glucagón puede revertir la esteatosis hepática y mejorar la intolerancia a la glucosa.
- INSP3R1 emerge como un objetivo terapéutico potencial para la enfermedad hepática grasa no alcohólica y la diabetes tipo 2.
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