Scientists have discovered a "gluttony gene" that may be responsible for obesity cases caused by compulsive non-stop eating.
In laboratory tests on mice, researchers discovered the Bdnf gene mutation failed to transmit the message to the brain that signals when the body is full.
The researchers hope the findings, published online in the journal Nature Medicine, could help with the treatment of obesity.
"This discovery may open up novel strategies to help the brain control body weight," said lead researcher Dr Baoki Xu, from Georgetown University Medical Centre in the US, as cited by the Press Association.
Two key hormones, leptin and insulin, release chemical signals that activate neurons in the hypothalamus region of the brain to signal when the body is satiated.
In the mice that had a mutation of the Bdnf gene, the neurons were not activated and therefore their food cravings continued. As a result, the mice ate twice as much as those without the mutation.
"If there is a problem with the Bdnf gene, neurons can't talk to each other and the leptin and insulin signals are ineffective, and appetite is not modified," said Dr Xu.
"Short" versions of the Bdnf gene block the leptin and insulin signals and prevent the "stop eating" message passing through the brain to the correct appetite-suppressing locations, say the scientists.
Previous studies have shown that mice without a 'long' version of this gene also suffered from memory impairment.
A link has also been previously identified between Bdnf mutations and obesity in humans.
Dr Xu said the next step was to look into the development of drugs that stimulate Bdnf activity in the brain.
"We have opened the door to both new avenues in basic research and clinical therapies, which is very exciting," he added.
Prof Sadaf Farooqi, who studies the relationship between genes and obesity at the University of Cambridge, told the BBC: "Genes have a surprisingly large role, it's often underestimated. Between 40 and 70% of the difference in weight between two individuals is due to genetics."
However, she added that the gene mutation is "very rare" in humans.