The brain region in question is the melanocortin system. It is already known that this system receives messages from the gut indicating whether it is hungry or full. The system responds by causing the body to either take in or burn calories.
This latest piece of research reveals that the melanocortin system is also responsible for controlling whether extra energy should be converted to fat and whether it should be stored or metabolised.
Experiments in rats showed that when the system is stimulated to increase activity, fat is metabolised. When activity levels in the system are reduced, fat accumulation increases. All of this happens independently of levels of food intake.
"We were able, in essence, to change traffic signals in so-called nutrient highways in the body so that calories were metabolised, and not dumped into fat cells, and we did this without changing the rate of food intake," explains Matthias Tschöp, Associate Professor of Psychiatry at the University of Cincinnati, who led the research.
The team also studied people who suffer from obesity caused by a genetic defect in the melanocortin system. The results indicated that the problem was caused by a fault in the fat storage/burning mechanism.
"Our results do not just explain why reduced levels of melanocortin can lead to overweight, even without increased food intake, but they indicate new targets for the development of effective medicines for controlling overweight," said Professor Tschöp. "These are urgently needed if we are to overcome the problem of obesity which is growing around the world."
EU funding for the work came from the Sixth Framework Programme DIABESITY project, which is looking for novel molecular targets for obesity and type 2 diabetes. Earlier this year, researchers from the project identified a molecule which contributes to obesity by providing the link between spontaneous physical activity, such as fidgeting whilst working at a computer, and food intake.
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