Recent tests have shown that switching off the satiety neurons caused mice to eat more and double their weight in three weeks. When the cells’ function was restored, the mice reduced the amount they ate each day by about 25pc.
Scientists found the cells in a small brain region called the paraventricular nucleus, which was already known to send and receive signals related to appetite and food intake.
Dr Richard Huganir, director of the Department of Neuroscience at Johns Hopkins University School of Medicine, said: “When the type of brain cell we discovered fires and sends off signals, our laboratory mice stop eating soon after.
“The signals seem to tell the mice they’ve had enough.”
A particular enzyme, OGT, was found to play a key role in the process by stimulating synaptic connections between the cells.
When the gene for OGT was silenced, the mice over-ate. Although they consumed the same number of meals as normal mice, they ate bigger portions.
Measurements of neuronal electrical activity showed that without OGT the cells lacked synaptic input.
“That result suggests that, in these cells, OGT helps maintain synapses,” said Dr Huganir.
“The number of synapses on these cells was so low that they probably aren’t receiving enough input to fire. In turn, that suggests that these cells are responsible for sending the message to stop eating.”
The findings are published in the latest edition of the journal Science.
Co-author Olof Lagerlof, a PhD student in Dr Huganir’s laboratory, said: “There are still many things about this system that we don’t know, but we think that glucose works with OGT in these cells to control ‘portion size’ for the mice.
“We believe we have found a new receiver of information that directly affects brain activity and feeding behaviour, and if our findings bear out in other animals, including people, they may advance the search for drugs or other means of controlling appetites.”