These 3 neurons may underlie the drive to eat food

The drive to eat may be controlled by a very simple circuit in the brain, new research in mice suggests.

Just three types of brain cells collaborate to suppress or enhance appetite, driving mice to eat less or more food, the study found.

First, specialized neurons detect "hunger-signaling hormones" that say whether an animal is full or hungry. These neurons then control the activity of neurons in a different part of the brain, which in turn, controls a third set of neurons in the jaw: These final nerve cells direct the movements needed for chewing.

The three-part circuit acts like a reflex, without needing conscious thought to direct it — similar to yanking your hand away from a hot object. In this case, the stimulus that sets off the reflex is a hunger-signaling hormone, and the resulting action is moving the jaw to chew.

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The new study, published Oct. 23 in the journal Nature, included only mice, and the three-part circuit has yet to be identified in humans. However, if it is found in people, this discovery could "change the narrative" on obesity, the authors behind the study argue.

"The control of how much we eat and when we eat is not so much based on your decision process, it just happens — it's a simple circuit," Christin Kosse, lead study author and a research associate at The Rockefeller University in New York, told Live Science.

In recent decades, medical organizations have characterized obesity as a chronic disease with an array of causes, including genetics. Previously, it was considered to be simply a consequence of personal decisions around eating. The new study adds evidence to the idea that physiological differences underlie obesity.

The new research also helps tie a number of existing theories about hunger together.

The first is known as "set point theory." Some scientists think that people generally have a body weight set point determined by their genetics and their environment. As the theory goes, a person's body tries to keep weight constant, even if they eat more or less food than they need — as such, there are various physiological mechanisms that help adjust for these fluctuations in calories.

But if these mechanisms fail, people may gain or lose weight.

For instance, after a filling meal, fat cells and cells in the gut release hunger-controlling hormones that signal to the brain that you should stop eating. These signals kick in approximately 20 minutes after you eat enough to be satiated. However, if this hormone signaling is disrupted for some reason, people can become extremely hungry even when they've eaten enough. In some cases, this can drive people to overeat to the point of becoming severely obese.

Previous research has shown that neurons in part of the brain called the hypothalamus play a role in regulating appetite, and they are targeted by weight-loss drugs in the same class as Ozempic. In addition, reductions in a protein called brain-derived neurotrophic factor (BDNF) in the brain are associated with obesity in both animals and humans.

The new study connects the dots between these findings.

In their experiments, Kosse and colleagues discovered that neurons in the hypothalamus that make BDNF are activated in the brains of mice who became obese after being fed a high-fat diet. This implies that these BDNF-making neurons activate in response to weight gain in order to suppress the rodents' appetites.

To test this hypothesis, the team switched these BDNF neurons on and off. When the neurons stopped working, the mice ate about 1200% more food than they normally would, and they made chewing movements even when there wasn't any food available to them. In some cases, they even started attempting to eat objects, such as wooden blocks, suggesting that this response was automatic.

Conversely, when the neurons were turned on, the opposite effect happened: The mice stopped eating and also didn't make any chewing movements. Once the team realized these BDNF neurons flip a key switch in the brain, they identified the two other types of neurons involved in this circuit.

Kosse believes that it is likely that we humans have a comparable control system for hunger in our brains.

Moving forward, the team now wants to see if this circuit changes in the context of different emotional states, such as anxiety.

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