In experiments on mice, researchers at the University of Pennsylvania in the US found that using deep brain stimulation reduced the animals' desire to overeat. It could have the same effect on humans, they hoped.
"Doing brain surgery for treating obesity is a controversial idea. However, binge eating is a common feature of obese patients that frequently is associated with suboptimal treatment outcomes," study author Dr Casey Halpern was quoted as saying by the Daily Mail.
The treatment is already approved for certain neurologic and psychiatric disorders, such as Parkinson's disease, and the procedure does not destroy any part of the brain and typically does not cause pain, he said.
According to the researchers, available treatments of obesity didn't adequately address the neural basis of compulsive overeating that often led to obesity.
A region of the brain called the nucleus accumbens is known to be dysregulated in both rodents and people who binge eat. Therefore, Halpern and his team targeted that region with deep brain stimulation in a strain of obesity prone mice.
The procedure involved implanting an electrode in the nucleus accumbens. Wires connected the electrode to an external neurostimulator, a device similar to a pacemaker.
When switched on, the stimulator triggers the electrode to deliver continuous electrical pulses to the brain.
After recovery from surgery, the mice received high-fat food at the same time every day for one hour, and the team measured their food consumption. For a week, mice consistently binged, eating almost half of their daily calories during this one hour, the authors reported.
Then on alternating days, the investigators turned on the stimulator. On the days that deep brain stimulation was administered, the team observed a significant (approximately 60 per cent) decrease in consumption of the high-fat diet. On the alternate days when they turned off the stimulator, binge eating returned.
By regulating various nerve cell receptors with medications the team discovered that the stimulation probably worked by affecting the type 2 dopamine receptor.
