The mystery of how some people can eat and never put on weight while others struggle to shed a single ounce may have finally been solved by scientists.

Slight differences in a single gene may be responsible for suppressing the metabolism, making its carriers permanently sluggish and unable to burn calories as effectively.

In contrast, thinner people seem to use up energy more rapidly, expending it in excess heat.

Scientists have long suspected that genetic differences were responsible for weight gain and singled out the FTO gene as the main culprit.

People with a high-risk version of the gene weigh on average three kilograms more than those with a low-risk version.

But they could not understand how it worked, theorising that it could influence appetite and food intake.

Now it appears the gene may control the rate of the metabolism. In experiments on mice those with the FTO gene entirely, were found to remain lean.

The scientists, led by Dr Ulrich Ruther, from the University of Düsseldorf in Germany, found the mice remained thin despite eating large amounts of food and being inactive.

The research, reported in the journal Nature, suggested the mice were burning up energy faster than animals with a functioning FTO gene.

It is thought the gene may limit the amount of energy given off in the form of heat.

Professor Stephen O'Rahilly, a metabolism expert from Cambridge University, said: "Genetic variation close to the FTO gene is definitely associated with obesity in humans, but, until now, it was not clear whether this genetic variation was likely to influence obesity by altering the expression or function of the FTO gene itself or some neighbouring gene.

"This work shows that if mice lack the FTO gene they are very lean because they spontaneously burn off enormous amounts of energy.

"This is a bit puzzling as several recent studies have suggested that the variant in the human FTO gene that increases the risk of obesity has effects on appetite and food intake but does not seem to have any effect on how quickly energy is burned off.

"So, this work provides a crucial piece of evidence supporting the notion that the FTO gene itself is likely to be involved in the effects of common human genetic variants on body fat."

The breakthrough could herald a raft of new treatments for obesity.

Dr Ruther added: "This finding will promote research into the development of drugs that modulate FTO activity. We strongly suspect that, in man, FTO might have more complex effects on both food intake and energy expenditure than has been so far suggested and that it is still not clear what the overall effect of inhibiting FTO in humans would be."