Scientists Discover the Obesity Gene Linked to Increased Weight Gain

First Posted: May 23, 2014 09:14 AM EDT
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Could there be a gene for obesity? Apparently, there is. Scientists have discovered that a gene commonly linked to obesity, called FTO, can contribute to weight gain. The findings could potentially help the fight against the increased rates of obesity across the world.

Since 2007, researchers have known that common variants in the fat mass and obesity-associated protein gene, FTO, are associated with increased weight in adults. But until now, scientists have been unsure how alterations in FTO could contribute to obesity. That's why researchers decided to investigate a bit further.

The scientists studied mice and found that as FTO expression increased or decreased, so did the expression of a nearby gene, RPGRIP 1L. This gene is known to play a role in regulating the primary cilium, and aberrations in cilium have been implicated in rare forms of obesity.

"If our findings are confirmed, they could explain how common genetic variants in the gene FTO affect body weight and lead to obesity," said Rudolph Leibel, one of the researchers, in a news release. "The better we can understand the molecular machinery of obesity, the better we will be able to manipulate these mechanisms and help people lose weight."

In fact, the researchers took their findings a step further to see what role RPGRIP 1L played in obesity. They created mice lacking one of their two RPGRIP 1L genes, reducing but not eliminating the gene's function. They found that mice lacking one of the RPGRIP 1L genes ate more food, gained more weight, and had a higher percentage of body fat. Essentially, FTO affected the expression of RPGRIP 1L which, in turn, affected bodyweight.

The findings reveal a bit more about the role of these genes in obesity. This, in turn, could open the door to future research to help prevent obesity. This is especially important as waistlines continue to grow across the globe.

The findings are published in the journal Cell Metabolism.

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