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Researchers hope to use the new information about the KLF14 gene to control type 2 diabetes and obesity  (Source:
A study of 800 UK female twins shows that the mother's copy of the gene provides the ability to control other genes associated with metabolic traits

Researchers from the University of Oxford and King's College London have made a crucial discovery that could lead to the development of better treatments and maybe even a cure for type 2 diabetes and obesity.

Professor Tim Spector, study leader from the Department of Twin Research at King's College London, and Professor Mark McCarthy, co-author of the University of Oxford, have determined how a previously discovered gene that is linked to type 2 diabetes and cholesterol acts as a regulator for the gene's that reside within the body's fat. 

KLF14 has been linked to type 2 diabetes and cholesterol levels in previous studies. But now, scientists have figured out how this gene acts as a regulator for genes located in far-away body fat.

"KLF14 seems to act as a master switch controlling processes that connect changes in the behavior of subcutaneous fat to disturbances in muscle and liver that contribute to diabetes and other conditions," said McCarthy. "We are working hard right now to understand these processes and how we can use this information to improve treatment of these conditions." 

A child inherits a set of genes from both the mother and the father. In this study, researchers found that the KLF14 gene inherited its activity from the mother while the father's KLF14 gene remains inactive. The KLF14's ability to control distant genes in the body's fat is completely dependent on the mother's version. 

They discovered that the mother's KLF14 gene controls other genes associated with body-mass index (obesity), insulin, glucose levels and cholesterol. This means that KLF14 is a "master switch" that controls and shows the connections between metabolic traits.

Researchers made this discovery by recruiting 800 UK female twin participants and studying over 20,000 genes in subcutaneous fat biopsies. They also looked at genes in subcutaneous fat biopsies from Icelandic participants. Between the two studies, researchers discovered the connections between the KLF14 gene and distant genes associated with metabolic traits.  

"This is the first major study that shows how small changes in one master regulator gene can cause a cascade of other metabolic effects in other genes," said Spector. "This has great therapeutic potential particularly as by studying large detailed populations such as the twins we hope to find more of these regulators." 

This study was published in Nature Genetics, and is part of multinational collaboration funded by the Wellcome Trust called the MuTHER study. 

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RE: news flash
By KingofFah on 5/18/2011 10:25:57 AM , Rating: 3
Yes, I'm aware of the ATP and the Krebs cycle. You're still not getting it. You also haven't understood what I've meant by 60%, and I'm not repeating it a third time.

It is incorrect that more fibre == more ATP required to contract. The body does not and almost never activates all fibres in a muscle. Also, during the majority of activity, a significant portion of work produced is generated by tendon work (far more efficient than muscle) in collaboration with the muscles. I give you kudos for examining it and trying to find an equation which explains your viewpoint, but you're missing too many factors in your equation to draw any meaningful conclusion -- again, tip of the iceberg.

I also just thought of something funny. Let's assume your more fibre == more ATP requirement equation is correct. The body rarely if ever goes through muscle fibre hyperplasia, so the amount of muscle fibres one has is basically determined through genes and cannot be modified after initial development. If your equation were true, then those who had more muscle fibres would be burning more energy at a given task, and subsequently, those who had less muscle fibres would be burning less energy. Do you understand why I find this funny? :) If not please think about it, as it's tremendously ironic.

Since you're very knowledgeable about this subject, I want to ask you something I've always wanted to know about muscle energy generation. What is the efficiency of an enlarged muscle fibre in comparison to a smaller muscle fibre, doing a load which is half of the smaller fibre's maximum work load? Essentially I wanted to know if a larger/stronger muscle fibre is capable of being more efficient than the smaller one at the same load.

As another factor to consider, research has shown BMR variances between two individuals of up to 2k calories. Even assuming that they burn exactly the same amount in other activities, there would be around 2k difference in their totals for the day, wouldn't there? :)

In the end, I really don't care whether you believe me or not, partly because you've demonstrated a lack of knowledge in this field to make an educated judgement, but mostly because it doesn't matter. It will never be not true for me, as I know I did it; and it will probably never be true for you as you have no proof, have no real way to get proof in this specific case, and are unlikely to actually research the field and ask questions in an explorative way since it would mean yielding that maybe you don't know what you're talking about.

Finally, your assumption that I write "page-long" comments to try to bring validity to what I type is incorrect. The most probable reason why I write "page-long" comments is because I rarely engage in internet discussions (and broke my own rule by doing so in trying to support the other "slow" metabolism people) and as such responded as best as I could in this very limited and disconnected discussion medium. I love discussing things in person. Hopefully you can understand that at least.

"We don't know how to make a $500 computer that's not a piece of junk." -- Apple CEO Steve Jobs

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