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Increasing Levels of Adiponectin Hormone Could Help Reverse Progression of Duchenne MD, Study Suggests

May 15, 2017

Increasing the levels of a muscle-inflammation-reducing hormone called adiponectin could help reverse the progression of Duchenne muscular dystrophy (DMD), a study suggests.

The article in the American Journal of Pathology was titled “Potential Therapeutic Action of Adiponectin in Duchenne Muscular Dystrophy.

Adiponectin can reduce acute and chronic muscle inflammation. Previous studies have shown that increasing its expression can prevent or delay DMD progression by decreasing inflammation-related muscle damage and improving muscle strength. Expression is the process by which information from a gene is used to create a functional product like a protein.

“We have previously shown that [adiponectin] could be a preventive agent powerful enough to counterbalance severe inflammation/oxidative stress and grave muscle damage in dystrophic muscles” of a mouse model of DMD, the researchers wrote.

The team decided to created a DMD mouse model that lacked adiponectin to investigate whether the deficiency worsened their symptoms. They also wanted to see if increasing the mice’s levels of adiponectin could reverse muscle abnormalities.

They discovered that DMD mice which lacked adiponectin had lower muscle force and endurance and more muscle damage than mice with DMD only. That finding suggested that adiponectin plays an important role in muscle health.

Importantly, using an adiponectin gene to trigger expression of the hormone led to significant reductions in muscle inflammation and damage markers, and promoted the expression of muscle regeneration molecules. Restoring adiponectin production markedly reduced the activity of NF-kB, a protein that plays a key role in inflammation.

Together, the findings support the notion that adiponectin helps protect muscle tissue and could help reverse the progression of the disease. This means adiponectin could become a way to treat DMD.

“[W]e showed that administration of [adiponectin], once mid-stage dystrophic lesions [muscular injuries or sores] are established, is able to reverse the disease, thereby strengthening the idea of a potential therapeutic role for this hormone,” the researchers wrote.

They called for studies that test whether boys with Duchenne DM have low adiponectin levels, which would validate their study’s findings. If the boys do have low levels of the hormone, then it would be important to see whether adiponectin may reverse the symptoms of their disease. Duchenne MD occurs primarily in boys.

“This study will help us to better understand [adiponectin] actions in regard to muscle protection, and hopefully will pave the way toward a novel pharmacological approach for neuromuscular disorders,” the researchers wrote.