26 March 2012
ByAppeared in BioNews 650
After eating, hormones send signals to the brain to let it know it's full. However, scientists found that in mice with a faulty version of the BDNF gene, these messages were 'blocked'.
'If there is a problem with the BDNF gene, neurons can't talk to each other, and the leptin and insulin [hormone] signals are ineffective, and appetite is not modified', said researcher Professor Baoji Xu from the Georgetown Medical Centre in the USA.
When the team monitored the eating habits of mice with and without the mutation, they found males were twice as heavy as their normal counterparts, and females were 2.7 times heavier. This was to do with them over-eating, rather than a reduction in their activity levels.
An additional part of the study, published in Nature Medicine, looked at what happened when leptin, often referred to as the 'hunger hormone' due to its role in regulating appetite, was injected into the mice. While the hormone had no effect on the mice with the BDNF mutation, there was a 26 percent reduction in amount of food eaten in those with a non-mutated gene.
The researchers now hope to use these results to help control obesity in humans.
Professor Xu said: 'This discovery may open up novel strategies to help the brain control body weight'.
However, any future treatment is still a long way off. Although we do have the BDNF gene, the mutation examined in this study is rare in humans and it cannot be assumed that human bodies react in exactly the same way as mice.
Tam Fry, spokesman for the National Obesity Forum, told the Daily Mail that 'fixing the mutation may not be plain sailing' and 'even when its fixed in mice it will be years before his solution can he be used in humans'.