- Researchers have identified a group of specialised neurons in the brainstem that regulate when to stop eating.
- These neurons track each bite, integrating multiple signals from food intake, gut hormones, and sensory cues.
- The discovery could lead to new treatments for obesity by targeting these neurons to control appetite.
For decades, scientists have studied the brain circuits involved in eating, but the exact mechanism that signals when a meal should end has remained elusive.
Now, researchers at Columbia University Irving Medical Center have identified a group of neurons in the brainstem that appear to make the final decision to stop eating.
Published in Nature, their findings suggest that these neurons track food intake and integrate multiple signals from the body before sending the command to cease eating.
This breakthrough could pave the way for new treatments for obesity and appetite-related disorders.
While previous research has shown that various brain circuits monitor food intake, those circuits do not appear to make the final decision on when to stop eating.
The newly discovered neurons, located in the brainstem, function as a control centre, using multiple types of sensory and hormonal information to regulate meal size.
Dr Alexander Nectow, who led the research, explains: “These neurons are unlike any others involved in regulating satiation. Other neurons typically sense food in the mouth, stomach fullness, or nutritional intake. These neurons integrate all this information and more to determine when to stop eating.”
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The decision to stop eating is something everyone experiences daily. At some point during a meal, we begin to feel full, and then we reach a moment where we stop eating entirely.
But how does the brain reach this conclusion?
To investigate, researchers used spatially resolved molecular profiling, a technique that allows them to identify specific cell types within a brain region. By focusing on the brainstem, they found a previously unrecognised set of neurons that had similarities to those involved in appetite regulation.
To determine the role of these neurons, the researchers engineered them to be controlled with light, allowing them to activate or deactivate the neurons at will.
When the neurons were activated:
- Mice ate significantly smaller meals.
- The intensity of activation influenced how quickly they stopped eating.
- Instead of stopping immediately, the mice slowed their eating before ceasing entirely.
The team also studied how other known appetite-related circuits and hormones affected these neurons. They found that:
- The neurons were silenced by ghrelin, a hormone that stimulates appetite.
- They were activated by GLP-1 agonists, a class of drugs currently used to treat obesity and diabetes.
- The neurons tracked each bite taken, incorporating sensory and hormonal information before determining when to stop eating.
According to Nectow, these neurons “smell food, see food, feel food in the mouth and gut, and interpret gut hormones released during eating. Ultimately, they process all this information to decide when enough is enough.”
Although the study was conducted in mice, the neurons were found in the brainstem, one of the oldest and most evolutionarily conserved parts of the brain. This suggests that humans likely have the same neurons, making this a promising target for obesity research.
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Dr Nectow believes that these findings could be the foundation for future obesity therapies: “This is a major new entry point to understanding what it means to feel full and how the brain controls meal size. We hope this discovery will lead to new treatments for obesity and related disorders.”
By targeting these neurons, scientists may develop new treatments that help people regulate their food intake more effectively.
The next step is to explore whether these neurons function similarly in humans and to investigate how they could be modulated for therapeutic use.
If successful, this research could transform our understanding of appetite regulation and lead to innovative treatments that help manage obesity, overeating, and metabolic disorders.
