Does beta-Hydroxy-beta-Methylbutyrate Have Any Potential to Support the Treatment of Duchenne Muscular Dystrophy in Humans and Animals?

Skeletal muscle is the protein reservoir of our body and an important regulator of glucose and lipid homeostasis. The dystrophin gene is the largest gene and has a key role in skeletal muscle construction and function. Mutations in the dystrophin gene cause Duchenne and Becker muscular dystrophy in humans, mice, dogs, and cats. Duchenne muscular dystrophy (DMD) is an X-linked neuromuscular condition causing progressive muscle weakness and premature death. fi-hydroxy fi-methylbutyrate (HMB) prevents deleterious muscle responses under pathological conditions, including tumor and chronic steroid therapy-related muscle losses. The use of HMB as a dietary supplement allows for increasing lean weight gain; has a positive immunostimulatory effect; is associated with decreased mortality; and attenuates sarcopenia in elderly animals and individuals. This study aimed to identify some genes, metabolic pathways, and biological processes which are common for DMD and HMB based on existing literature and then discuss the consequences of that interaction.

Automated summary

Skeletal muscle serves as a protein reservoir and plays a crucial role in regulating glucose and lipid homeostasis. Mutations in the dystrophin gene cause muscular dystrophy, a neuromuscular condition characterized by progressive muscle weakness and shortened lifespan. The use of HMB, a dietary supplement, has shown promising effects in preventing muscle loss and improving overall health in pathological conditions. This study aims to identify common genes, metabolic pathways, and biological processes between DMD and HMB, and discuss their interaction and consequences.