July 16, 2013
Researchers Discover How Genetic Mutation Leads To Obesity
redOrbit Staff & Wire Reports - Your Universe Online
A gene mutation previously linked to obesity causes people to have elevated levels of a "hunger hormone" in their blood, causing their appetite to return shortly after eating, according to new research appearing in the Journal of Clinical Investigation.
The variant, which occurs in what is known as the FTO gene, has also been linked to increased activity in regions of the brain linked to appetite control and reward when shown pictures of appealing food, researchers from University College London (UCL) have discovered.
According to Telegraph Science Correspondent Nick Collins, their findings could help explain why individuals with this high-risk variant have larger appetites and tend to consume higher calorie foods.
The scientists studied 359 male patients who either had two copies of the high-risk FTO gene, or two copies of a genetic variant believed to be associated with a low risk of obesity. Levels of the hunger hormone, which is known as ghrelin, typically fall after eating and remove a person's feelings of hunger, Collins said.
However, blood samples from 20 of the study participants showed those with the variation did not suppress the hormone like usual. The researchers also conducted a series of post-meal brain scans which also showed men with the high-risk genes found pictures of fatty foods more appealing than low-risk patients.
In addition to solving the mystery of how the genetic variant can increase obesity risk, the study could help researchers develop treatments that target ghrelin in order to help reduce weight gain, explained BBC News Health and Science Reporter James Gallagher.
"There is a strong family link with obesity, and a person's genetic code is thought to play a major role in the risk of them becoming overweight," Gallagher said. "People have two copies of the FTO gene - one from each parent - and each copy comes in a high and a low-risk form. Those with two-high risk copies of the FTO gene are thought to be 70 percent more likely to become obese than those with low-risk genes. But no-one knew why."
The link between the FTO gene variant and increased risk of obesity was first described in the journal Science back in 2007. However, UCL's Rachel Batterham, the leader of the new study, told Reuters reporter Ben Hirschler their research shows the mutation is actually "a double hit" because of the way it increases both ghrelin levels and the brain's sensitivity to the chemical.
Batterham, who heads up the university's center for obesity research, also told BBC News patients with the gene variants are "biologically programmed to eat more" and their brains are "set up to be particularly interested in anything to do with high-calorie food." She also recommended those seeking to lower their ghrelin levels should consider exercise such as cycling, and eat more meals that are high in protein.
According to Daily Mail Science Correspondent Fiona Macrae, 16 percent of people in the UK have two rogue copies of the FTO gene, and consume an average of 200 extra calories per day. In addition, nearly half (49 percent) of individuals have one flawed FTO gene, and those people are 30 percent more likely to be obese than those who do not possess the gene mutations, she added.