Scientists have identified two new populations of cells in the brain that regulate appetite and may help develop drugs to treat obesity by controlling hunger signals.
"Obesity is generally associated with leptin resistance and our recent data suggest that modulation of the activity of specific neurons with drugs could bypass leptin resistance and provide a new means for reducing body weight," said Jeffrey Friedman, professor at Rockefeller University in the US.
Researchers located the two types of cells in a part of the brainstem called the dorsal raphe nucleus.
The team zeroed in on the dorsal raphe nucleus, or DRN, when a whole-brain imaging revealed that this part of the brain becomes activated in hungry mice.
Subsequent imaging of other mice that were fed more than their normal amount of food, until they were full, revealed a different pattern of DRN activity.
These results indicated quite clearly that neurons in that part of the brain played a role in feeding behaviour, researchers said.
They then determined which of the several types of neurons that make up the DRN were involved.
Genetic analysis of the activated cells in the two groups of mice showed that the neurons triggered by a full belly released glutamate, a chemical that nerve cells use to signal one another, while the neurons triggered by hunger released a different neurotransmitter, known as GABA.
"There are two possibilities when you see something like that. One is that the cells are just along for the ride, they are getting activated by hunger but they are not actually driving the food intake process," said Alexander Nectow from Rockefeller University.
"The other possibility is that they are in fact part of the sense and respond mechanism to hunger and in this case, we suspected the latter," Nectow added.
Researchers were able to turn on the glutamate-releasing cells in obese mice. This suppressed the animals' food intake and made them lose weight. It also confirmed that the DRN neurons turned on by hunger did indeed drive food intake.
Similarly, flipping on the GABA-releasing neurons in the same part of the brain had the opposite effect and increased food intake.
Turning on the "hunger neurons" automatically turned off the "satiety neurons," maximising the effect, researchers said.
They also studied the effect of switching off hunger neurons in obese mice.
"We were excited to see that prolonged inhibition of these neurons could dramatically reduce body weight," said Marc Schneeberger Pane, postdoctoral fellow at Rockefeller University.
The findings open up new avenues of research into exactly how the brain controls eating, and suggest that drugs designed to activate or inhibit neurons in the DRN could be effective in treating obesity and preventing its related disorders, such as diabetes and hypertension, researchers said.
The study was published in the journal Cell.
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