The mystery of a genetic flaw which greatly increases the risk of obesity in one in six people has been solved by an international group of scientists. A version of an obesity gene, called FTO, had been linked to a bigger belly, but the reason why was uncertain. A study, published in The Journal of Clinical Investigation, showed it made fatty foods more tempting and altered levels of the hunger hormone, ghrelin.
Obesity experts said drugs targeting ghrelin might reduce weight gain.
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.
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 be70% more likely to become obese than those with low-risk genes.
But no-one knew why.
Hormonal
A team, led by researchers at University College London, tested two groups of men. All were a normal weight, but one group had the high-risk FTO genes and the other was low risk.
The first tests looked at levels of the hormone ghrelin either side of a meal in 10 men from each group.
Levels of the hormone, which makes people hungry, did not fall as far in the high-risk patients after the meal. Their ghrelin levels also began to climb more quickly.
In separate tests, a series of brain scans after a meal showed further differences between the two groups. Men with the high-risk genes found pictures of high-fat foods more appealing than the low-risk men.
Dr Rachel Batterham, the head of the centre for obesity research at University College London, told the BBC News website: “Their brain is set up to be particularly interested in anything to do with high-calorie food.”
She said they were “biologically programmed to eat more”.
Help?
Dr Batterham said understanding how FTO affected the odds of becoming overweight would help patients.
She said exercise such as cycling was an excellent way to lower ghrelin levels and there was a significant amount of research from pharmaceutical companies working on the hormone.
She added: “Also protein meals do lower ghrelin more, so anything that suppresses ghrelin is more likely to be effective in FTO patients.”
The FTO mutations were probably life-saving at one point in human history when piling on the pounds in the summer would help people survive the winter.
Commenting on the findings, Prof Steve Bloom, from Imperial College London, said: “We know the tendency to overeat in a society with too much food and no need for exercise is inherited.
“Slowly we are discovering the factors which make us overweight and this study, encompassing not only demonstration of a higher level of hunger hormone, ghrelin, but also changes in the brain associated with ghrelin’s action, is an important step forward.”
The study was funded by the Rosetrees Trust and the Medical Research Council.
