Re: Tweaking a gene makes muscles twice as strong

[Guest guest]

Question:

Ok so the muscles are twice as strong...but can the bones handle all this?

I mean, aging can result in osteopenia and other wasting of the bones, right?

When supposedly healthy folks are now breaking arms bench pressing due to

increased loads on the bones - perhaps this is something they should consider?

if the change in the muscle is not sufficiently gradual to allow the bones to

build OR the bones are unable to build, then perhaps this won't be a good way to

sort out sarcopenia?

The Phantom

aka Schaefer, CMT/RMT, competing powerlifter

Denver, Colorado, USA

Tweaking a gene makes muscles twice as strong

Tweaking a gene makes muscles twice as strong

A team of researchers at EPFL, the University of Lausanne and the Salk Institute

created super strong, marathon mice and nematodes by reducing the function of a

natural inhibitor, suggesting treatments for age-related or genetically caused

muscle degeneration are within reach.

It turns out that a tiny inhibitor may be responsible for how strong and

powerful our muscles can be. This is the surprising conclusion reached by

scientists in EPFL's Laboratory of Integrative Systems Physiology (LISP), in

collaboration with a group in the Center for Integrative Genomics at the

University of Lausanne and at the Salk Institute in California. By acting on a

receptor (NCoR1), they were able to modulate the transcription of certain genes,

creating a strain of mighty mice whose muscles were twice a strong as those of

normal mice.

Two protein-building regulators

The process of transcription, in which proteins are manufactured by an organism

in response to instructions contained in its DNA, is modulated by co-factors.

These either favor (coactivators) or inhibit (corepressors) transcription, in

principle by responding to the concentration of certain hormones in the body,

which are in turn associated with the organism's environment.

In an article appearing today in the journal Cell, a team led by EPFL professor

Johan Auwerx reports on the results of experiments done in parallel on mice and

nematodes. By genetically manipulating the offspring of these species, the

researchers were able to suppress the NCoR1 corepressor, which normally acts to

inhibit the buildup of muscle tissues.

Better muscles

In the absence of the inhibitor, the muscle tissue developed much more

effectively. The mice with the mutation became true marathoners, capable of

running faster and longer before showing any signs of fatigue. In fact, they

were able to cover almost twice the distance run by mice that hadn't received

the treatment. They also exhibited better cold tolerance.

Unlike previous experiments with so-called super mice, this study addresses the

way energy is burned in the muscle and the way the muscle is built. Examination

under a microscope confirmed that the muscle fibers of the modified mice are

denser, the muscles are more massive, and the cells in the tissue contain higher

numbers of mitochondria--cellular organelles that deliver energy to the muscles.

Similar results were also observed in nematode worms, allowing the scientists to

conclude that their results could be applicable to a large range of living

creatures.

Obese but not diabetic

According to a second article published in the same journal and also involving

EPFL's LISP Laboratory, suppressing the NCoR1 receptor in adipose tissues (fat)

also led to interesting results. By acting on this corepressor, it was possible

to fundamentally change the corpulence of the mice being studied without

inducing weight-related diseases. " The specimens that became obese via this

treatment did not suffer from diabetes, unlike mice who become obese for other

reasons, " notes Auwerx.

The scientists have not yet detected any deleterious side effects associated

with eliminating the NCoR1 receptor from muscle and fat tissues, and although

the experiments involved genetic manipulations, the researchers are already

investigating potential drug molecules that could be used to reduce the

receptor's effectiveness.

Treating degeneration

The researchers say their results are a milestone in our understanding of

certain fundamental mechanisms of living organisms, in particular the

little-studied role of corepressors. In addition, they give a glimpse at

possible long-term therapeutic applications. " This could be used to combat

muscle weakness in the elderly, which leads to falls and contributes to

hospitalizations, " emphasizes Auwerx. " In addition, we think that this could be

used as a basis for developing a treatment for genetic muscular dystrophy. "

If these results are confirmed in humans, there's no question it will attract

interest from athletes as well as medical experts. " It will be important for

anti-doping authorities to monitor that these treatments are not used in an

unauthorized manner, " concludes Auwerx.

============================

Mice which were genetically altered were able to run almost 50 per cent further

and for 20 minutes longer than their normal cousins.

http://www.telegraph.co.uk/science/science-news/8881342/Scientists-tweak-gene-to\

-create-mighty-mouse.html

Although the mice developed slightly larger muscles, they did not need to eat

any more than usual and were virtually indistinguishable from the outside other

than by their vastly improved endurance.

The study, published in the Cell journal, could help scientists develop drugs to

keep the muscles healthy in old age and find treatments for muscle-wasting

diseases.

The researchers, from the University of Lausanne and the EPFL University in

Switzerland, were not the first to produce " mighty mice " but said their work

held greater potential for medical research.

While previous studies have focused on improving the way muscles use glucose –

giving them much more explosive power – the latest experiment used a different

gene which controls the way they burn fatty acids.

This meant the mice could improve their muscle performance for a longer period

simply by burning more body fat, without requiring vast amounts of food to keep

up their glucose supply.

Prof Johan Auwerx, who led the research, said: " If you are thinking about

glucose you are talking about the sprinting muscles – we are talking about the

marathon muscles.

" This is not like a sledgehammer or an on-off switch, it is like a dimmer. If

you want to treat a patient you do not want to make a superman, you want to

protect the muscle so it does not degrade. "

========

Carruthers

Wakefield, uk

[Guest guest]

Question:

Ok so the muscles are twice as strong...but can the bones handle all this?

I mean, aging can result in osteopenia and other wasting of the bones, right?

When supposedly healthy folks are now breaking arms bench pressing due to

increased loads on the bones - perhaps this is something they should consider?

if the change in the muscle is not sufficiently gradual to allow the bones to

build OR the bones are unable to build, then perhaps this won't be a good way to

sort out sarcopenia?

The Phantom

aka Schaefer, CMT/RMT, competing powerlifter

Denver, Colorado, USA

Tweaking a gene makes muscles twice as strong

Tweaking a gene makes muscles twice as strong

A team of researchers at EPFL, the University of Lausanne and the Salk Institute

created super strong, marathon mice and nematodes by reducing the function of a

natural inhibitor, suggesting treatments for age-related or genetically caused

muscle degeneration are within reach.

It turns out that a tiny inhibitor may be responsible for how strong and

powerful our muscles can be. This is the surprising conclusion reached by

scientists in EPFL's Laboratory of Integrative Systems Physiology (LISP), in

collaboration with a group in the Center for Integrative Genomics at the

University of Lausanne and at the Salk Institute in California. By acting on a

receptor (NCoR1), they were able to modulate the transcription of certain genes,

creating a strain of mighty mice whose muscles were twice a strong as those of

normal mice.

Two protein-building regulators

The process of transcription, in which proteins are manufactured by an organism

in response to instructions contained in its DNA, is modulated by co-factors.

These either favor (coactivators) or inhibit (corepressors) transcription, in

principle by responding to the concentration of certain hormones in the body,

which are in turn associated with the organism's environment.

In an article appearing today in the journal Cell, a team led by EPFL professor

Johan Auwerx reports on the results of experiments done in parallel on mice and

nematodes. By genetically manipulating the offspring of these species, the

researchers were able to suppress the NCoR1 corepressor, which normally acts to

inhibit the buildup of muscle tissues.

Better muscles

In the absence of the inhibitor, the muscle tissue developed much more

effectively. The mice with the mutation became true marathoners, capable of

running faster and longer before showing any signs of fatigue. In fact, they

were able to cover almost twice the distance run by mice that hadn't received

the treatment. They also exhibited better cold tolerance.

Unlike previous experiments with so-called super mice, this study addresses the

way energy is burned in the muscle and the way the muscle is built. Examination

under a microscope confirmed that the muscle fibers of the modified mice are

denser, the muscles are more massive, and the cells in the tissue contain higher

numbers of mitochondria--cellular organelles that deliver energy to the muscles.

Similar results were also observed in nematode worms, allowing the scientists to

conclude that their results could be applicable to a large range of living

creatures.

Obese but not diabetic

According to a second article published in the same journal and also involving

EPFL's LISP Laboratory, suppressing the NCoR1 receptor in adipose tissues (fat)

also led to interesting results. By acting on this corepressor, it was possible

to fundamentally change the corpulence of the mice being studied without

inducing weight-related diseases. " The specimens that became obese via this

treatment did not suffer from diabetes, unlike mice who become obese for other

reasons, " notes Auwerx.

The scientists have not yet detected any deleterious side effects associated

with eliminating the NCoR1 receptor from muscle and fat tissues, and although

the experiments involved genetic manipulations, the researchers are already

investigating potential drug molecules that could be used to reduce the

receptor's effectiveness.

Treating degeneration

The researchers say their results are a milestone in our understanding of

certain fundamental mechanisms of living organisms, in particular the

little-studied role of corepressors. In addition, they give a glimpse at

possible long-term therapeutic applications. " This could be used to combat

muscle weakness in the elderly, which leads to falls and contributes to

hospitalizations, " emphasizes Auwerx. " In addition, we think that this could be

used as a basis for developing a treatment for genetic muscular dystrophy. "

If these results are confirmed in humans, there's no question it will attract

interest from athletes as well as medical experts. " It will be important for

anti-doping authorities to monitor that these treatments are not used in an

unauthorized manner, " concludes Auwerx.

============================

Mice which were genetically altered were able to run almost 50 per cent further

and for 20 minutes longer than their normal cousins.

http://www.telegraph.co.uk/science/science-news/8881342/Scientists-tweak-gene-to\

-create-mighty-mouse.html

Although the mice developed slightly larger muscles, they did not need to eat

any more than usual and were virtually indistinguishable from the outside other

than by their vastly improved endurance.

The study, published in the Cell journal, could help scientists develop drugs to

keep the muscles healthy in old age and find treatments for muscle-wasting

diseases.

The researchers, from the University of Lausanne and the EPFL University in

Switzerland, were not the first to produce " mighty mice " but said their work

held greater potential for medical research.

While previous studies have focused on improving the way muscles use glucose –

giving them much more explosive power – the latest experiment used a different

gene which controls the way they burn fatty acids.

This meant the mice could improve their muscle performance for a longer period

simply by burning more body fat, without requiring vast amounts of food to keep

up their glucose supply.

Prof Johan Auwerx, who led the research, said: " If you are thinking about

glucose you are talking about the sprinting muscles – we are talking about the

marathon muscles.

" This is not like a sledgehammer or an on-off switch, it is like a dimmer. If

you want to treat a patient you do not want to make a superman, you want to

protect the muscle so it does not degrade. "

========

Carruthers

Wakefield, uk

[Guest guest]

On Nov 13, 2011, at 12:14 PM, carruthersjam wrote:

> Tweaking a gene makes muscles twice as strong

>

Sounds a little like what happens in Belgian Blue cattle, but different, in the

cattle a mutation yields huge musculature, it sounds as tho' this genetic tweak

increases strength and endurance as opposed to size. Interesting if the two

could be put together in a human organism. The way things are moving along these

days, we'll probably be able to do this in 10 years if not a lot sooner.

Fair winds and happy bytes, Dave Flory, Flower Mound, TX

Speak softly and study Aikido, and you won't need to carry a big stick.

[Guest guest]

I wonder how long it will take for the supplement producers to market a " NCoR1

receptor blocker "

Ralph Giarnella MD

Southington Ct. USA 

________________________________

From: " deadliftdiva@... " <deadliftdiva@...>

Supertraining

Sent: Sunday, November 13, 2011 3:19 PM

Subject: Re: Tweaking a gene makes muscles twice as strong

 

Question:

Ok so the muscles are twice as strong...but can the bones handle all this?

I mean, aging can result in osteopenia and other wasting of the bones, right?

When supposedly healthy folks are now breaking arms bench pressing due to

increased loads on the bones - perhaps this is something they should consider?

if the change in the muscle is not sufficiently gradual to allow the bones to

build OR the bones are unable to build, then perhaps this won't be a good way to

sort out sarcopenia?

The Phantom

aka Schaefer, CMT/RMT, competing powerlifter

Denver, Colorado, USA

Tweaking a gene makes muscles twice as strong

Tweaking a gene makes muscles twice as strong

A team of researchers at EPFL, the University of Lausanne and the Salk Institute

created super strong, marathon mice and nematodes by reducing the function of a

natural inhibitor, suggesting treatments for age-related or genetically caused

muscle degeneration are within reach.

It turns out that a tiny inhibitor may be responsible for how strong and

powerful our muscles can be. This is the surprising conclusion reached by

scientists in EPFL's Laboratory of Integrative Systems Physiology (LISP), in

collaboration with a group in the Center for Integrative Genomics at the

University of Lausanne and at the Salk Institute in California. By acting on a

receptor (NCoR1), they were able to modulate the transcription of certain genes,

creating a strain of mighty mice whose muscles were twice a strong as those of

normal mice.

Two protein-building regulators

The process of transcription, in which proteins are manufactured by an organism

in response to instructions contained in its DNA, is modulated by co-factors.

These either favor (coactivators) or inhibit (corepressors) transcription, in

principle by responding to the concentration of certain hormones in the body,

which are in turn associated with the organism's environment.

In an article appearing today in the journal Cell, a team led by EPFL professor

Johan Auwerx reports on the results of experiments done in parallel on mice and

nematodes. By genetically manipulating the offspring of these species, the

researchers were able to suppress the NCoR1 corepressor, which normally acts to

inhibit the buildup of muscle tissues.

Better muscles

In the absence of the inhibitor, the muscle tissue developed much more

effectively. The mice with the mutation became true marathoners, capable of

running faster and longer before showing any signs of fatigue. In fact, they

were able to cover almost twice the distance run by mice that hadn't received

the treatment. They also exhibited better cold tolerance.

Unlike previous experiments with so-called super mice, this study addresses the

way energy is burned in the muscle and the way the muscle is built. Examination

under a microscope confirmed that the muscle fibers of the modified mice are

denser, the muscles are more massive, and the cells in the tissue contain higher

numbers of mitochondria--cellular organelles that deliver energy to the muscles.

Similar results were also observed in nematode worms, allowing the scientists to

conclude that their results could be applicable to a large range of living

creatures.

Obese but not diabetic

According to a second article published in the same journal and also involving

EPFL's LISP Laboratory, suppressing the NCoR1 receptor in adipose tissues (fat)

also led to interesting results. By acting on this corepressor, it was possible

to fundamentally change the corpulence of the mice being studied without

inducing weight-related diseases. " The specimens that became obese via this

treatment did not suffer from diabetes, unlike mice who become obese for other

reasons, " notes Auwerx.

The scientists have not yet detected any deleterious side effects associated

with eliminating the NCoR1 receptor from muscle and fat tissues, and although

the experiments involved genetic manipulations, the researchers are already

investigating potential drug molecules that could be used to reduce the

receptor's effectiveness.

Treating degeneration

The researchers say their results are a milestone in our understanding of

certain fundamental mechanisms of living organisms, in particular the

little-studied role of corepressors. In addition, they give a glimpse at

possible long-term therapeutic applications. " This could be used to combat

muscle weakness in the elderly, which leads to falls and contributes to

hospitalizations, " emphasizes Auwerx. " In addition, we think that this could be

used as a basis for developing a treatment for genetic muscular dystrophy. "

If these results are confirmed in humans, there's no question it will attract

interest from athletes as well as medical experts. " It will be important for

anti-doping authorities to monitor that these treatments are not used in an

unauthorized manner, " concludes Auwerx.

============================

Mice which were genetically altered were able to run almost 50 per cent further

and for 20 minutes longer than their normal cousins.

http://www.telegraph.co.uk/science/science-news/8881342/Scientists-tweak-gene-to\

-create-mighty-mouse.html

Although the mice developed slightly larger muscles, they did not need to eat

any more than usual and were virtually indistinguishable from the outside other

than by their vastly improved endurance.

The study, published in the Cell journal, could help scientists develop drugs to

keep the muscles healthy in old age and find treatments for muscle-wasting

diseases.

The researchers, from the University of Lausanne and the EPFL University in

Switzerland, were not the first to produce " mighty mice " but said their work

held greater potential for medical research.

While previous studies have focused on improving the way muscles use glucose –

giving them much more explosive power – the latest experiment used a different

gene which controls the way they burn fatty acids.

This meant the mice could improve their muscle performance for a longer period

simply by burning more body fat, without requiring vast amounts of food to keep

up their glucose supply.

Prof Johan Auwerx, who led the research, said: " If you are thinking about

glucose you are talking about the sprinting muscles – we are talking about the

marathon muscles.

" This is not like a sledgehammer or an on-off switch, it is like a dimmer. If

you want to treat a patient you do not want to make a superman, you want to

protect the muscle so it does not degrade. "

========

Carruthers

Wakefield, uk

[Guest guest]

I wonder how long it will take for the supplement producers to market a " NCoR1

receptor blocker "

Ralph Giarnella MD

Southington Ct. USA 

________________________________

From: " deadliftdiva@... " <deadliftdiva@...>

Supertraining

Sent: Sunday, November 13, 2011 3:19 PM

Subject: Re: Tweaking a gene makes muscles twice as strong

 

Question:

Ok so the muscles are twice as strong...but can the bones handle all this?

I mean, aging can result in osteopenia and other wasting of the bones, right?

When supposedly healthy folks are now breaking arms bench pressing due to

increased loads on the bones - perhaps this is something they should consider?

if the change in the muscle is not sufficiently gradual to allow the bones to

build OR the bones are unable to build, then perhaps this won't be a good way to

sort out sarcopenia?

The Phantom

aka Schaefer, CMT/RMT, competing powerlifter

Denver, Colorado, USA

Tweaking a gene makes muscles twice as strong

Tweaking a gene makes muscles twice as strong

A team of researchers at EPFL, the University of Lausanne and the Salk Institute

created super strong, marathon mice and nematodes by reducing the function of a

natural inhibitor, suggesting treatments for age-related or genetically caused

muscle degeneration are within reach.

It turns out that a tiny inhibitor may be responsible for how strong and

powerful our muscles can be. This is the surprising conclusion reached by

scientists in EPFL's Laboratory of Integrative Systems Physiology (LISP), in

collaboration with a group in the Center for Integrative Genomics at the

University of Lausanne and at the Salk Institute in California. By acting on a

receptor (NCoR1), they were able to modulate the transcription of certain genes,

creating a strain of mighty mice whose muscles were twice a strong as those of

normal mice.

Two protein-building regulators

The process of transcription, in which proteins are manufactured by an organism

in response to instructions contained in its DNA, is modulated by co-factors.

These either favor (coactivators) or inhibit (corepressors) transcription, in

principle by responding to the concentration of certain hormones in the body,

which are in turn associated with the organism's environment.

In an article appearing today in the journal Cell, a team led by EPFL professor

Johan Auwerx reports on the results of experiments done in parallel on mice and

nematodes. By genetically manipulating the offspring of these species, the

researchers were able to suppress the NCoR1 corepressor, which normally acts to

inhibit the buildup of muscle tissues.

Better muscles

In the absence of the inhibitor, the muscle tissue developed much more

effectively. The mice with the mutation became true marathoners, capable of

running faster and longer before showing any signs of fatigue. In fact, they

were able to cover almost twice the distance run by mice that hadn't received

the treatment. They also exhibited better cold tolerance.

Unlike previous experiments with so-called super mice, this study addresses the

way energy is burned in the muscle and the way the muscle is built. Examination

under a microscope confirmed that the muscle fibers of the modified mice are

denser, the muscles are more massive, and the cells in the tissue contain higher

numbers of mitochondria--cellular organelles that deliver energy to the muscles.

Similar results were also observed in nematode worms, allowing the scientists to

conclude that their results could be applicable to a large range of living

creatures.

Obese but not diabetic

According to a second article published in the same journal and also involving

EPFL's LISP Laboratory, suppressing the NCoR1 receptor in adipose tissues (fat)

also led to interesting results. By acting on this corepressor, it was possible

to fundamentally change the corpulence of the mice being studied without

inducing weight-related diseases. " The specimens that became obese via this

treatment did not suffer from diabetes, unlike mice who become obese for other

reasons, " notes Auwerx.

The scientists have not yet detected any deleterious side effects associated

with eliminating the NCoR1 receptor from muscle and fat tissues, and although

the experiments involved genetic manipulations, the researchers are already

investigating potential drug molecules that could be used to reduce the

receptor's effectiveness.

Treating degeneration

The researchers say their results are a milestone in our understanding of

certain fundamental mechanisms of living organisms, in particular the

little-studied role of corepressors. In addition, they give a glimpse at

possible long-term therapeutic applications. " This could be used to combat

muscle weakness in the elderly, which leads to falls and contributes to

hospitalizations, " emphasizes Auwerx. " In addition, we think that this could be

used as a basis for developing a treatment for genetic muscular dystrophy. "

If these results are confirmed in humans, there's no question it will attract

interest from athletes as well as medical experts. " It will be important for

anti-doping authorities to monitor that these treatments are not used in an

unauthorized manner, " concludes Auwerx.

============================

Mice which were genetically altered were able to run almost 50 per cent further

and for 20 minutes longer than their normal cousins.

http://www.telegraph.co.uk/science/science-news/8881342/Scientists-tweak-gene-to\

-create-mighty-mouse.html

Although the mice developed slightly larger muscles, they did not need to eat

any more than usual and were virtually indistinguishable from the outside other

than by their vastly improved endurance.

The study, published in the Cell journal, could help scientists develop drugs to

keep the muscles healthy in old age and find treatments for muscle-wasting

diseases.

The researchers, from the University of Lausanne and the EPFL University in

Switzerland, were not the first to produce " mighty mice " but said their work

held greater potential for medical research.

While previous studies have focused on improving the way muscles use glucose –

giving them much more explosive power – the latest experiment used a different

gene which controls the way they burn fatty acids.

This meant the mice could improve their muscle performance for a longer period

simply by burning more body fat, without requiring vast amounts of food to keep

up their glucose supply.

Prof Johan Auwerx, who led the research, said: " If you are thinking about

glucose you are talking about the sprinting muscles – we are talking about the

marathon muscles.

" This is not like a sledgehammer or an on-off switch, it is like a dimmer. If

you want to treat a patient you do not want to make a superman, you want to

protect the muscle so it does not degrade. "

========

Carruthers

Wakefield, uk

[Guest guest]

As I continue to age and explore my non-athleticism, I'm wondering if I have a

gene to tweak. It sure is an adventure trying to work with whatever I've got.

Anyway when they're ready to do a pilot study on humans - sign me up!

 

Regards,

Plisk

Excelsior Sports

Buffalo NY

Prepare To Be A Champion!