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FTO comes in two varieties or “alleles”, and everyone inherits two copies of the gene, one from each parent. The team found that people who inherit two copies of one variant — 16 per cent of white Europeans — were 70 per cent more likely to be obese than those who inherited two copies of the other allele. The 50 per cent of subjects who inherited one copy of each FTO variant had a 30 per cent higher risk of obesity.

Those in the highest risk group weighed an average of 3kg more and those at medium risk were an average of 1.2kg heavier. In each case, the extra weight was entirely accounted for by more body fat, not greater muscle or extra height. The results, which are published in the journal Science apply to both men and women, and to children as young as seven.

FTO will not be the only gene that influences obesity, and inheriting a particular variant will not necessarily make anyone fat. “There are going to be lots of slim people with two copies of the bad allele, and if people who have the more favourable version overeat or don’t exercise they are still going to become obese,” Professor McCarthy said. “This is not a gene for obesity, it is a gene that contributes to risk.”

The biological function of FTO remains unknown, and the scientists now plan to study this by creating genetically modified mice in which the gene is knocked out.

Professor McCarthy said the gene is highly active in the hypothalamus, a part of the brain involved in appetite control, suggesting that one potential way it might have its effect. The gene could also influence how readily fat cells are laid down.

The research involved too many people to control for exercise and diet, so it is not yet known whether FTO affects how much people eat or how active they are. Andrew Hattersley, who headed the Exeter group, said it might nevertheless explain how people with apparently similar lifestyles differ in their propensity to put on weight.

“Our findings suggest a possible answer to someone who might ask: ‘I eat the same and do as much exercise as my friend next door, so why am I fatter?’” he said. “There is clearly a component to obesity that is genetic.”

Professor McCarthy played down the idea of screening people for FTO, so they can change their diet or exercise habits if they are found to be at higher risk. “We are not pushing genetic testing here. A 3kg increase is significant, but it is not 30kg, and there are always going to be other genes and environmental factors involved. The best way of predicting who is becoming obese is to weigh them.”

Independent obesity experts said the discovery was highly significant. Susan Jebb of the MRC Human Nutrition Unit said: “This research provides clear evidence of a biological mechanism which makes some people more susceptible to gaining weight in a world where food is plentiful and sedentary lifestyles the norm. By studying the action of this gene we may learn more about the detailed causes of obesity.”

Professor Steve O’Rahilly of Cambridge said: “It is unlikely to be the only such genetic variant, but it is the first to be discovered. Unfortunately we have no idea what this gene actually does to alter our degree of fatness. It is made in every cell in the body and doesn’t look like any genes whose functions we understand so we have very few clues as to how it might affect a person’s risk of obesity. This is a very exciting first step but there is much work still to do.”

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