Some of our brains are better at it than others'. Suzanne Tucker/Shutterstock

You don’t have to be a brain surgeon to know when you’ve had enough to eat, but a team of neuroscientists from Canada and Germany has now figured out how the stomach communicates with the central nervous system in order to tell us to stop shoveling food into our mouths.

The first breakthrough on this subject came back in the 90s, when researchers discovered that a hormone called leptin is secreted into the bloodstream by fat cells in order to signal that the stomach is full. However, how this hormone gets from the blood into the brain has remained something of a mystery.

The main point of contact between the bloodstream and the hypothalamus – a brain region involved in controlling appetite, among other things – is known as the median eminence (ME). Here, compounds in the blood come into contact with neurons, although this process can be risky, since the blood also carries waste products and other harmful substances that could potentially damage these neurons.

Fortunately, the ME is loaded with a type of cell known as NG2-glia, which helps to protect neurons by stimulating the production of the myelin sheath that coats them. Noticing that NG2-glia are more numerous in the ME than elsewhere in the brain, the study authors began to speculate that it may play a key role in allowing safe contact between leptin and the neurons of the hypothalamus.

“We think that the NG2-glia cells act to support and shelter the leptin receptor neurons, enabling them to instruct the body when to stop eating,” explained study co-author Maia Kokoeva.

To investigate, they chemically deactivated the NG2-glia cells in the ME of mice, and found that this instantly caused them to start overeating – to the point where some of them doubled in weight in just one month.

Hungry for confirmation of their results, which are published in the journal Cell Metabolism, the researchers then genetically engineered mice to lack microglia – another type of brain cell that helps to protect neurons. Noting that this produced no changes in the animals’ weight or eating habits, they were able to state with confidence that it is indeed the NG-glia, and not the microglia, that enables neurons to receive leptin.

Taking the experiment a step further, the team then targeted the NG2-glia of mice using X-irradiation, which is similar to the radiotherapy used to treat brain tumors. Once again, this caused the mice to gorge themselves and become obese.

According to Kokoeva, “people who have been treated for brain tumors using radiation to block cell proliferation often become overweight.” The results of this study may therefore provide an explanation for this, suggesting that “the reason for this weight gain may be the loss of NG2-glia in the median eminence as a result of radiation.”

Without these vital brain cells, then, we’d literally spend our entire time eating without ever feeling full or slumping into a food coma – which actually sounds quite appealing.