'Gluttony gene’ may be behind big appetites
Monday 19 March 2012
A single gene's effect on the brain can result in non-stop eating, research has shown.
Scientists believe the "gluttony gene" may be responsible for cases of obesity caused by out-of-control appetite.
The Bdnf gene variant was studied in mice. It was found to prevent brain neurons from transmitting signals that tell the body it has eaten enough.
"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.
Hunger and satiety, the sensation of "feeling full", are governed by a complex balance of hormonal and neuronal signals.
Two hormones in particular, leptin and insulin, released in the body after a meal play a key role.
Their chemical signals activate neurons in the hypothalamus region of the brain that trigger satiety. But if the connection is not made, the craving for food continues.
"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.
The research is reported online in the journal Nature Medicine.
Bdnf makes a protein that is synthesised in dendrites, the branch-like "fingers" that project from nerve cells. Dendrites carry the synapses that neurons use to communicate to each other.
"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.
Previous work by Dr Xu has shown that Bdnf is important for the formation and maturation of synapses during development.
Mice born without the correct "long" version of the gene suffer impaired learning and memory. They also grow to be severely obese.
Other researchers conducting large-scale genome comparison studies found a link between Bdnf mutations and obesity in humans.
The research opens up the possibility of tackling obesity by using drugs that stimulate Bdnf activity in the brain, said Dr Xu.
"We have opened the door to both new avenues in basic research and clinical therapies, which is very exciting," he added.
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