
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 be 70% 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.
Source:
http://dld.bz/cHPuu