Scientists find how obesity gene works, a clue to treatment

[Najinsky]

They should speak to McDonalds. McD clearly already have the technology to transfer this gene mutation via synthetic food, evidenced by the growth in fat Thais since McD's arrival here.

[Grouse]

It does not matter whether it works or not. Belief is the key point. Note the researchers are going for a patent (on the gene?). No doubt billions will be made. Altruism? I think not...

[partington]

It does not matter whether it works or not. Belief is the key point. Note the researchers are going for a patent (on the gene?). No doubt billions will be made. Altruism? I think not...

Are plumbers altruistic when they fix your toilet?

At the risk of adding too much information here's a simpler version of that almost impenetrable scientific jargon in case anyone is interested in what has actually been done.

In the human gene called FTO ( a gene is a long stream of DNA code letters, A,T, G or C that tells the body how to make a protein) there is a region that does not code for a protein. All genes are made up of regions that code and regions that don't.

Some people (around 56% of caucasians ) have a letter C in the region of FTO that does not code for a protein, and some people have a T there (around 44% of caucasians). Just this simple letter difference that is very common has a major effect on your likelihood of becoming obese. This work has found out why this is so, and proved it.

When there is a T in that bit of the FTO DNA, a protein called ARIDB5 attaches itself directly to it, and then has a big effect on genes around that site. When ARIDB5 binds to this bit of FTO, it prevents two other genes called IRX3 and IRX5 making their proteins (also called IRX3 and IRX5).

Now IRX3 and IRX5 are proteins that control whether fat cells become white or brown

They do this because they activate a set of genes that tell cells to "become white fat cells". When you do not make enough IRX3 and IRX5 , this tells your cells "become brown fat cells". Brown fat cells are good because they do not store fat, they burn it off to produce heat.

So when you have a C in that place in the FTO gene, ARIDB5 does not attach itself, and so the proteins IRX3 and IRX5 are made in large amounts. This causes the body to make white fat (bad= obesity) rather than brown fat (good=burns off calories).

They have tested this in mice and human cells by making the animals or cells increase the amount of ARIDB5, IRX3 or IRX5 they make, and by adjusting the C to a T in fat cells taken from a "C" person and showing that these cells now behave like brown not white fat. This is not a matter of belief - the conclusions are really well proven.

It is not often that scientists call other scientists' work "a tour de force" , which is how this study has been described. Whether it will ever produce a drug is unknown - but it is a place to start.

[Jingthing]

Sure, some day some people are going to get very rich indeed on an effective medical treatment (and prevention) for obesity. So what? Many people are ALREADY getting very rich selling massively INEFFECTIVE solutions! In fact, they bank on their plans not working, because better customers who constantly fail for life than offering something that actually works.

The fact that scientific advances will get corrupted by commercial interests is a legitimate issue, but it doesn't make the pursuit of scientific breakthroughs worthless either.

So get the science right first ... then when there finally is a much more effective treatment to offer, then it probably gets political and economic. Because there are many major nations who have a lot to lose by not addressing the obesity epidemic in their populations.

U.S. military officials have even suggested it is a matter of national security. Not enough fit young people.

Now in case in future a massively effective medical tweak is developed AND it is very expensive, then it will inevitably get VERY politicized, and rightly so. Because it will be mean that no rich people will be obese and all the obese people will be among the poor.

Edited August 21, 2015 by Jingthing

[HooHaa]

now if they could only pinpoint the moob and beer gut genes bangkok would be a better place

[Neurath]

It does not matter whether it works or not. Belief is the key point. Note the researchers are going for a patent (on the gene?). No doubt billions will be made. Altruism? I think not...

Are plumbers altruistic when they fix your toilet?

At the risk of adding too much information here's a simpler version of that almost impenetrable scientific jargon in case anyone is interested in what has actually been done.

In the human gene called FTO ( a gene is a long stream of DNA code letters, A,T, G or C that tells the body how to make a protein) there is a region that does not code for a protein. All genes are made up of regions that code and regions that don't.

Some people (around 56% of caucasians ) have a letter C in the region of FTO that does not code for a protein, and some people have a T there (around 44% of caucasians). Just this simple letter difference that is very common has a major effect on your likelihood of becoming obese. This work has found out why this is so, and proved it.

When there is a T in that bit of the FTO DNA, a protein called ARIDB5 attaches itself directly to it, and then has a big effect on genes around that site. When ARIDB5 binds to this bit of FTO, it prevents two other genes called IRX3 and IRX5 making their proteins (also called IRX3 and IRX5).

Now IRX3 and IRX5 are proteins that control whether fat cells become white or brown

They do this because they activate a set of genes that tell cells to "become white fat cells". When you do not make enough IRX3 and IRX5 , this tells your cells "become brown fat cells". Brown fat cells are good because they do not store fat, they burn it off to produce heat.

So when you have a C in that place in the FTO gene, ARIDB5 does not attach itself, and so the proteins IRX3 and IRX5 are made in large amounts. This causes the body to make white fat (bad= obesity) rather than brown fat (good=burns off calories).

They have tested this in mice and human cells by making the animals or cells increase the amount of ARIDB5, IRX3 or IRX5 they make, and by adjusting the C to a T in fat cells taken from a "C" person and showing that these cells now behave like brown not white fat. This is not a matter of belief - the conclusions are really well proven.

It is not often that scientists call other scientists' work "a tour de force" , which is how this study has been described. Whether it will ever produce a drug is unknown - but it is a place to start.

Now I'm confused:

"The accumulated data across seven independent studies therefore clearly implicates the FTO gene in humans as having a direct impact on food intake but no effect on energy expenditure."

[partington]

It does not matter whether it works or not. Belief is the key point. Note the researchers are going for a patent (on the gene?). No doubt billions will be made. Altruism? I think not...

Are plumbers altruistic when they fix your toilet?

At the risk of adding too much information here's a simpler version of that almost impenetrable scientific jargon in case anyone is interested in what has actually been done.

In the human gene called FTO ( a gene is a long stream of DNA code letters, A,T, G or C that tells the body how to make a protein) there is a region that does not code for a protein. All genes are made up of regions that code and regions that don't.

Some people (around 56% of caucasians ) have a letter C in the region of FTO that does not code for a protein, and some people have a T there (around 44% of caucasians). Just this simple letter difference that is very common has a major effect on your likelihood of becoming obese. This work has found out why this is so, and proved it.

When there is a T in that bit of the FTO DNA, a protein called ARIDB5 attaches itself directly to it, and then has a big effect on genes around that site. When ARIDB5 binds to this bit of FTO, it prevents two other genes called IRX3 and IRX5 making their proteins (also called IRX3 and IRX5).

Now IRX3 and IRX5 are proteins that control whether fat cells become white or brown

They do this because they activate a set of genes that tell cells to "become white fat cells". When you do not make enough IRX3 and IRX5 , this tells your cells "become brown fat cells". Brown fat cells are good because they do not store fat, they burn it off to produce heat.

So when you have a C in that place in the FTO gene, ARIDB5 does not attach itself, and so the proteins IRX3 and IRX5 are made in large amounts. This causes the body to make white fat (bad= obesity) rather than brown fat (good=burns off calories).

They have tested this in mice and human cells by making the animals or cells increase the amount of ARIDB5, IRX3 or IRX5 they make, and by adjusting the C to a T in fat cells taken from a "C" person and showing that these cells now behave like brown not white fat. This is not a matter of belief - the conclusions are really well proven.

It is not often that scientists call other scientists' work "a tour de force" , which is how this study has been described. Whether it will ever produce a drug is unknown - but it is a place to start.

Now I'm confused:

"The accumulated data across seven independent studies therefore clearly implicates the FTO gene in humans as having a direct impact on food intake but no effect on energy expenditure."

You don't give any source or attribution for this quote, but a search shows it's from the wikipedia article on FTO, which is not up to date.

The section you quote is not very well expressed and so inaccurate. The C to T variant discussed in the OP is called rs1421085. Of the "seven Independent studies" mentioned in the wikipedia article, six looked at rs9939609 , a completely different variation, and one looked at rs17817449 and rs1421085. So each study cannot be extrapolated to the whole FTO gene, and only tell you about the effects of these single letter changes.

Therefore only one study looked at the actual C/T variation involved in the OP, the other six were looking at different single letter changes. The study that did look at rs1421085 found that this was associated with resting metabolic rate, but when the difference in fat free body mass between people was taken into account this association disappeared. They mention themselves that they cannot tell whether this is because the rs1421085 variant causes people to have more fat free mass, (which would be the case if the C/T change is causing less white fat to form).

So all the studies mentioned in wiki save one are looking at a different place, and the one that is looking at the C/T finds a difference in resting metabolic rate but is unable to say from their results if it's definitely caused by the C/T variation.

No discrepancy with current results therefore.

Edited August 21, 2015 by partington

[up-country_sinclair]

I propose the following experiment:

Put some of these fatties in a cage for 3 months and only give them 2000 calories of healthy food if they do 30 minutes of exercise.

Weigh them before and after, and I'd bet every single one of them leaves thinner.

I'm not saying that genetics don't play a role, but the majority of these fat slobs are gluttons with no self control or self respect. They need to take a look in the mirror if they are searching for something / someone to blame. OK, maybe two mirrors, side by side.

Edited August 21, 2015 by up-country_sinclair

[Satcommlee]

I think these Scientists want to come round to local Mom and Pop shop and examine the beer fridge there... That is without doubt a cause of obesity!

[Jingthing]

A current article related to the OP's topic:

http://edition.cnn.com/2016/02/01/health/new-protein-fat-burn-feat/index.html

A lot of information about the key being a specific protein: sLR11

According to Vidal-Puig, obese people have less brown fat than lean people -- and the same applies for diabetics. "If you can increase the brown fat in obese and diabetic people then you can improve their situation," says Vidal-Puig. This has been known for some time, but making it a reality has been a challenge.

My question is this. Is there any practical way to INCREASE brown fat cells (the good kind) that we can do now? I don't think there is, but asking.

[trogers]

The ability to store energy as fat would be extraordinarily useful in a feast-famine environment, and people with this gene would have been selected over those burning the the energy rather than storing it. Would be interesting to see the historical and geographical distribution of the genetic traits. Genes distributed at different rates (environmentally determined) in all populations and environments so as to ensure that not all would be wiped out by famine like conditions.

Have yet to see a fat starving African with defective genes...

Perhaps eating too much from a young age causes genes to be defective?