In addition, researchers at the American Diabetes and Obesity Center of Excellence found that
blocking myostatin raises the body's sensitivity to leptin, the satiety hormone, which helps curb hunger more efficiently in terms of a reduced - calorie diet.
To determine whether the FLRG transgene was causing increased muscle growth by
blocking myostatin activity, I examined the effect of combining the FLRG transgene with a loss - of - function mutation in the myostatin gene.
The drug, which is currently in clinical trials,
blocks myostatin — and perhaps GDF11 as well.
Of course, there is a lot more research needed for this to be anywhere close to relevant to our normal daily lives, but this experiment proves that it is indeed possible to create a quick drug that would
block our myostatin production and allow us to mimic the effects of exercise on our bodies, even when we're not moving off the couch.
Not exact matches
I have presented data showing that FLRG, like follistatin, can promote muscle growth when expressed as a transgene in skeletal muscle and that both of these molecules appear to act by
blocking not only
myostatin but also other ligands with similar activity to
myostatin.
Exercise restores decreased physical activity levels and increases markers of autophagy and oxidative capacity in
myostatin / activin -
blocked mdx mice.
It is the flip - side of
myostatin, as increased follistatin
blocks the activity of
myostatin: either increased follistatin or reduced
myostatin produce similar outcomes in animal studies, with treated individuals demonstrating increased muscle mass.
Of course, we've known about
myostatin for a while now, and we knew that if we somehow succeeded in
blocking it, we could have amazing muscle gains with reduced gym time, as well as significantly reduced risk of heart or kidney illnesses.
Researchers found that when
myostatin was absent in animals, or its action was
blocked, the animals displayed massive increases in muscle mass, and decreases in fat mass [1 - 9].