LONDON: Scientists have finally solved what they claim is the "fat gene" mystery, a key finding that sheds light on why some people can eat but
never put on weight while others struggle to shed flab.
Earlier studies suspected that genetic differences were responsible for weight gain and singled out the FTO gene as the main culprit.
Now, a team, led by Düsseldorf University in Germany, has found concrete evidence that the gene may control the rate of the metabolism, making its carriers leaner than those without it.
The scientists reached the conclusion after carrying out experiments on mice. Those with the FTO gene entirely were found to remain lean. The animals remained thin despite eating large amounts of food and being inactive, the 'Nature' journal reported in its latest edition.
According to the scientists, the breakthrough could herald a raft of new treatments for obesity.
"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," lead scientist Ulrich Ruther was quoted by 'The Daily Telegraph' as saying.
Experts have welcomed the research. 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 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."