The scientists believe the technique could prevent or even cure obesity in those people with the faulty gene and negate the effects of a high-fat diet.
“Obesity has traditionally been seen as the result of an imbalance between the amount of food we eat and how much we exercise, but this view ignores the contribution of genetics to each individual’s metabolism,” said senior author Professor Manolis Kellis, of MIT’s Computer Science and Artificial Intelligence Laboratory (CSAIL) and of the Broad Institute.
“Knowing the causal variant underlying the obesity association may allow genome editing as a therapeutic avenue for individuals as risk.
“By manipulating this new pathway, we could switch between energy storage and energy dissipation providing new hope for a cure against obesity.”
In Britain, 25 per cent of adults are obese — 12 million people — compared with fewer than three per cent in the Seventies. The proportion is predicted to grow to one in three by 2030 and more than half by 2050.
To test the theory that a faulty gene was driving weight gain, researchers gathered fat samples from Europeans carrying both the ‘obesity’ variant and a normal copy of the FTO gene.
They found that in people with the variant one letter of DNA code had been replaced by another. The wrong code was causing genes IRX3 and IRX5 to turn on when they should have been off.
Previous studies have shown that IRX3 and IRX5 switch on during times of fat loss in the body, such as during periods of starvation to conserve fat.
Researchers used a new technology called the Crispr/Cas9 system to edit the DNA code and repair the sequence in mice and human cells. The technique sees a modified protein (Cas9) injected into the body where it can snip away specific sections of DNA.
Mice which had been bred to obese saw a reduction of body weight and all major fat stores, and complete resistance to a high-fat diet.
The researchers are now looking at how to make the process useful for humans.
The research was published in the New England Journal of Medicine.