Published this week in the journal Proceedings of the National Academy of Sciences, the scientists found that inhibiting activin A, activin B and
myostatin resulted in skeletal muscle mass increase by as much as 150 per cent in preclinical models.
Not exact matches
There are interesting similarities between the
results of the current study and published data from leptin - deficient mice with genetic ablation of the atrophic hormone
myostatin (55, 56).
Conceivably, this maternal effect could
result from transfer of
myostatin or a downstream mediator either prenatally from the maternal to fetal circulations or postnatally from the mother to the offspring during nursing; in this respect,
myostatin mRNA has been reported to be expressed in the mammary gland of lactating pigs [24].
Taken together, these
results suggest that the maternal effect on muscle mass
results most likely from prenatal transfer of some mediator from mother to fetus, perhaps
myostatin itself.
This finding taken together with the
results of cross fostering experiments suggest that muscle mass can be influenced by prenatal transfer of some mediator from mother to fetus; although
myostatin itself is the most obvious candidate for this mediator, additional experiments will be required to prove this definitively.
Moreover, loss of
myostatin activity
resulting either from postnatal inactivation of the Mstn gene [3], [4] or following administration of various
myostatin inhibitors to wild type adult mice [5]--[7] can also lead to significant muscle growth.
As a
result, there has been considerable effort directed at developing strategies to modulate
myostatin activity in clinical settings where enhancing muscle growth may be beneficial.
In order to determine whether this effect of follistatin
results solely from inhibition of
myostatin activity, I analyzed the effect of this transgene in
myostatin - null mice.
As a
result of a number of natural animal lineages with this mutation,
myostatin knockout is by far the most examined and tested of all potential gene therapies.
Secondly, the study lasted just 2 weeks, and yes favorable
results were obtained, via an average change of +49.2 % (follistatin) to -16.6 % (
myostatin), however the study duration was far from sufficient to observe muscle growth differences.
It is also important to note that these
results were observed in middle aged people, who possess higher levels of
myostatin and lower follistatin to begin with.
It regulates
myostatin - signaling pathways, leading to lower action of
myostatin inhibition that
results in more muscle fiber building.
«Supplementation with creatine
resulted in greater increases in muscle mass and strength, and these improvements were accompanied by more decreased
myostatin levels.»
There are interesting similarities between the
results of the current study and published data from leptin - deficient mice with genetic ablation of the atrophic hormone
myostatin (55, 56).