New research into the role played by the FTO (fat-mass and obesity associated) gene in obesity has been published in the journal Nature, showing that the gene may function in metabolism.

The FTO gene has been linked to obesity in the past, which has provoked much interest in it. A previous study in the UK, reported in BioNews in December last year, noted a change in eating habits in children with a variant of the FTO gene. Children with the variant tended to choose to eat more energy-dense foods and on average ate 100 calories per meal more than children with the normal FTO gene.

This new study, carried out by scientists led by Dr Ulrich Ruther at the University of Dusseldorf, Germany, looked at mice with the FTO gene 'knocked out', so that there were no gene products. They found that, despite eating and exercising the same as normal mice, mice lacking the gene were leaner. The mice exhibited slowed growth after birth and less fat tissue, and by the age of six weeks they had 30 to 40 per cent less weight than normal mice.

Lean mass was also lower, but to a lesser extent. They also found changes in blood levels of some specific hormones; of particular interest were higher levels of adrenaline.

The authors explain that the results seen could be due to increased metabolism, a contrasting angle to the one suggested by previous work, which was that the gene affects food intake and appetite.

The work has thrown up many more questions that need to be answered, and shows that the interplay of processes in obesity is extremely complex. Dr Ruther says: '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'.

There is a hope that one day a drug could be developed to combat obesity, and these findings will help promote research into this. This is very far off, however, as Dr Ruther says that 'it is still not clear what the overall effect of inhibiting FTO in humans would be'.