Introducción

El propósito de este Estudio  fue examinar si la L-leucina (Leu), β-hidroxi-β-metilbutirato (HMB), o creatina monohidrato, evitaría posibles efectos atróficos provocados por la miostatina en el musculo esquelético. Para todo aquel que no sepa que función tiene la miostatina, la proteína miostatina (formalmente conocida como factor 8 de crecimiento y diferenciación) es un factor de crecimiento que limita el crecimiento del tejido muscular, por ejemplo concentraciones elevadas de miostatina en un individuo provocan una disminución en el desarrollo normal de los músculos. La proteína miostatina se produce en células del músculo esquelético, circula en sangre y actúa en el tejido muscular, al parecer retrasando el desarrollo de las células madre musculares. El mecanismo exacto sigue siendo desconocido. Hasta 2005, no hay drogas en el mercado que inhiban la Miostatina para los seres humanos, pero fue desarrollado un anticuerpo genéticamente modificado para reconocer la Miostatina y neutralizarla por la compañía farmacéutica de New-Jersey Wyeth. El inhibidor se llama MYO-029 y está actualmente en fase experimental en humanos. Algunos atletas, impacientes por conseguir tales drogas, buscan por Internet, donde se están vendiendo bloqueadores de la Miostatina falsos.

1550-2783-11-38-1Métodos

El tratamiento fué llevado a cabo por cuatro grupos, los cuales fuerón estudiados de la siguiente manera:

1) 3 veces por día mM Leu 10,

2) 3 veces por día HMB 10 mM,

3) 3x día mM Creatina 10, sólo

4) DM, grupo control.

Después del tratamiento, células como la proteína total, el contenido de ADN, el contenido de ARN, la síntesis de proteínas musculares (MPS) y el diámetro de la fibra, se analizarón exhaustivamente. Se analizarón los tratamientos por separado para los patrones de expresión de mRNA de los genes relacionados con la miostatina (Akirin-1 / Mighty, Notch-1, Esquí, MyoD), así como atrogenes (MuRF-1, y MAFbx / atrogina-1)

Resultados

NTCR diámetro de la fibra disminuyó aproximadamente un 30% en comparación con DM / miotubos CTL (p <0,001). Leu, HMB y Creatina podrían haber sido los responsables de prevenir la atrofia inducida por NTCR. NTCR no disminuyó los niveles de MPS en comparación con DM / miotubos CTL, pero el tratamiento NTCR disminuyó la expresión de ARNm de Akirin-1 / Mighty en un 27% (p <0,001) y MyoD en un 26% (p <0,01) en comparación con DM / miotubos CTL . Sorprendentemente, NTCR + Leu y NTCR + HMB miotubos tenían niveles Akirin-1 / Mighty y MyoD ARNm similares en comparación con DM / miotubos CTL.

 

Conclusión

Los investigadores demuestran como la administración de  L-leucina, HMB y creatina monohidrato puede revertir la atrofia inducida por miostatina en los miotubos; Potencialmente, esto resulta de la acción independiente de la modulación de cada ingrediente Akirin-1 / Mighty expresión de ARNm. Además, los resultados sugieren que, a pesar de los tratamientos NTCR, el tratamiento de monohidrato de creatina fué capaz de regular la ARNm Akirin-1 / Mighty lo que conduce a un efecto hipertrófico claramente independiente de la síntesis de proteína muscular. Futuro en estudios in vivo debe seguir examinando cómo leucina, HMB, y / o monohidrato de creatina de forma independiente o sinérgica afectan en la expresión genética de Akirin-1 / Mighty .

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