A gene called FTO was found to be related to obesity in 2007, but scientists have finally figured out how it makes people fat. This discovery could lead to a new approach to treating obesity beyond diet and exercise.
It appears that a faulty version of FTO causes energy from food to be stored as fat rather than burned as energy. This was found through genetic work on mice and in human cells in the lab. This work may mean that the action of the gene can be reversed.
The study was conducted by scientists at MIT and Harvard University and published in the New England Journal of Medicine.
The discovery of how FTO works means that for some people obesity is not, or not only, a matter of eating too much or exercising too little. Work on this gene could lead to a pathway for drugs that can make fat cells behave differently.
The FTO gene appears to influence body weight indirectly by affecting two other genes that control the burning off energy. There are two types of fat in the body. Brown or beige fatty tissue (the so-called "good fat") burns calories, while white fat stores them. The body constantly makes fat cells, and the two other genes determine if they become brown or white ones.
In other tests on human cells, blocking the gene's effect increased energy burning in fat cells. Editing out the problem gene in human cells in the lab also restored normal metabolic function. When researchers blocked the faulty gene's effect in mice, they found they became 50% leaner than other mice despite eating a high-fat diet, and that they burned more energy even when asleep.
The faulty gene does not appear to be a factor in all or most cases of obesity. The study found the gene in 44% of Europeans but only 5% of blacks.