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El corazón que falla depende de los cuerpos cetónicos como combustible

Gregory Aubert¹, Ola J Martin¹, Julie L Horton¹

¹From Cardiovascular Metabolism Program, Sanford Burnham Prebys Medical Discovery Institute, Orlando, FL (G.A., O.J.M., J.L.H., L.L., R.B.V., T.C.L., S.J.G., P.A.C., D.P.K.); Departments of Medicine, Pharmacology, and Cancer Biology, Duke University, Durham, NC (T.K., D.M.M.); CECAD Research Center, Institute for Genetics, University of Cologne, Cologne, Germany (M.K.); Departments of Pharmacology and Medicine, Case Western Reserve University, Cleveland, OH (C.L.H.); College of Medicine, University of Illinois at Chicago, Chicago, IL (E.D.L.); and Department of Medicine, Washington University School of Medicine, St. Louis, MO (P.A.C.).

|January 29, 2016

Resumen

El corazón que falla cambia a usar cuerpos cetónicos para obtener energía cuando disminuye la utilización de ácidos grasos. La identificación de estos cambios metabólicos en la insuficiencia cardíaca puede conducir a nuevos tratamientos.

Área de la Ciencia:

Cardiología
Investigación metabólica
La bioquímica

Sus antecedentes:

El corazón que falla se caracteriza por la falta de energía.
La utilización de los ácidos grasos, el principal combustible del corazón, disminuye durante la insuficiencia cardíaca.
La exploración de fuentes alternativas de combustible miocárdico es crucial para el desarrollo de terapias para la insuficiencia cardíaca.

Objetivo del estudio:

Investigar las alteraciones metabólicas de la energía en el corazón durante la hipertrofia y la insuficiencia cardíaca.
Para identificar cambios en las vías de utilización de combustible en los corazones que fallan.
Para descubrir nuevos objetivos terapéuticos para la insuficiencia cardíaca.

Principales métodos:

Proteómica mitocondrial cuantitativa en modelos de ratón de hipertrofia y insuficiencia cardíaca.
Estudios de resonancia magnética nuclear (RMN) ex vivo en preparaciones cardíacas aisladas.
Perfiles metabólicos cuantitativos específicos de muestras de miocardio basados en la espectrometría de masas.

Principales resultados:

Desregulación de las proteínas involucradas en la utilización de ácidos grasos en la insuficiencia cardíaca.
Aumento de la expresión de beta-hidroxibutirato deshidrogenasa 1, una enzima clave en la oxidación de las cetonas.
Cambio demostrado en la preferencia de combustible hacia los cuerpos cetónicos en corazones hipertrofiados y con insuficiencia, a pesar de la reducida capacidad de oxidación de los ácidos grasos.

Conclusiones:

El corazón hipertrofiado y fallido utiliza cuerpos cetónicos como una fuente significativa de combustible para la producción de ATP.
Se identificaron "biosignaturas" específicas del metabolito de la utilización de cetonas cardíacas in vivo.
Investigaciones adicionales sobre la naturaleza adaptativa o desadaptativa de este cambio de combustible podrían revelar nuevas estrategias terapéuticas para la insuficiencia cardíaca.

Palabras clave:

Ácidos grasos insuficiencia cardíaca hipertrofía el metabolismo Biología molecular

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