Wednesday, October 19, 2011

Genetic basis of obesity

Sanjena Sathian

So it looks like Raquel and I picked the same topic:

The really interesting thing about this study is that it demonstrates the smaller level at which molecular changes can impact phenotype and individuals' health. FTO is a gene that has been studied for a long time because of its potential links to obesity, type II diabetes and even some other problems including potentially Alzheimers, and funnily enough, webbed toes in mice.

This study has expanded on that FTO link, finding that the allele of FTO that has been linked to higher rates of obesity (or more specifically, larger appetite/propensity for food consumption) is involved in methylization of messenger RNA. This is something that we know happens to DNA a lot, where a certain protein's function is to remove a methyl (CH3) group from a DNA base. But here, it's happening with adenosine on messenger RNA; what's also unique here is that it's reverse methylization, so the FTO protein secreted by the obesity-risk-allele is actually capable of both removing and adding a methyl group to the adenosine base.

If researchers know something about this, they might be able to come up with new and innovative gene-therapy ways of treating lifelong obesity (though many previous studies have indicated that despite a propensity for consuming more, those with the risk-allele of FTO can still exercise and live healthily). In addition, it points to an important new field where studying what is happening even at the base level of RNA is important, so we have to go even smaller than exon splicing etc to understand genetic variation.

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