A group of researchers at Rockefeller University in New York have discovered a new solution for obesity in the form of hunger-controlling cells in the brain.
The research adds weight to evidence that eating is a surprisingly complex biological behaviour.
According to the researchers, there are two types of cells located in the dorsal raphe nuclear in the brainstem. These new cells are the potential targets for new drugs to treat obesity as it is believed that they can be manipulated to control the hunger signals that initiate the search and consumption of food.
Results indicate that neurons in this part of the brain play a major role in feeding behaviour.
“The recent data suggests that modulation of the activity of specific neurons with drugs could bypass leptin resistance and provide a new means for reducing body weight,” said another researcher Jeffrey Friedman.
Study author Alexander Nectow and his colleagues zeroed in on the dorsal raphe nucleus, or DRN, when whole-brain imaging made with iDISCO an advanced technique developed at Rockefeller revealed that this part of the brain becomes activated in hungry mice. Imaging other mice that were given more than their normal amount of food showed a different pattern of DRN activity. This showed that neurons in this part of the brain clearly had a function in feeding behaviour.
Further research is needed to ascertain which types of neurons that make up the DRN are involved in the process. “There are two possibilities when you see something like that,” Dr Nectow said.
“One is that the cells are just along for the ride – they are getting activated by hunger but they’re not actually driving the food intake process. The other possibility is that they are in fact part of the sense-and-respond mechanism to hunger – and in this case, we suspect the latter.”
Manipulating the system armed with two proven methods for activating targeted neurons at will – one optical, one chemical – the researchers were able to turn on the glutamate-releasing cells in obese mice. Similarly, flipping on the GABA-releasing neurons in the same part of the brain had the opposite effect and increased food intake. Notably, turning on the “hunger neurons” automatically turned off the “satiety neurons”, maximising the effect.
This article originally appeared on The Independent.
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