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New York, NY – Scientists at Columbia University have uncovered a unique group of neurons in the brainstem that command the body to stop eating. This discovery, made in mice, provides critical insights into the regulation of satiety and could pave the way for new obesity treatments.
Neurons That Sense Eating Behavior
The research, led by Alexander Nectow, a physician-scientist at Columbia University Vagelos College of Physicians and Surgeons, along with associate research scientist Srikanta Chowdhury, identified these neurons as key regulators of meal termination.
“These neurons are unlike any other involved in regulating satiation,” said Nectow. “They appear to integrate multiple signals related to food intake, including taste, gut distension, and nutrient absorption.”
Deciphering the End of a Meal
Humans and animals experience a moment during eating when they recognize they have had enough. While prior studies identified brain circuits monitoring food intake, they had not pinpointed the exact neurons responsible for ending a meal.
Using advanced single-cell techniques, including spatially resolved molecular profiling, Nectow’s team was able to observe the neurons in their natural environment and analyze their molecular composition. Their findings confirm that these cells are integral in controlling food intake.
Neurons and Eating Behavior
To determine the function of these neurons, the researchers used optogenetics, a technique that allows cells to be activated or deactivated by light. When these neurons were stimulated, the mice ate significantly smaller meals, suggesting that the neurons send signals that gradually slow down eating before completely stopping it.
“Interestingly, these neurons don’t just signal an immediate stop; they help the mice slow down their eating gradually,” said Chowdhury.
The study found that these neurons respond to various sensory cues from the mouth, gut, and visual perception of food, integrating these signals to determine when enough food has been consumed.
Interaction with Appetite-Regulating Hormones
Further research revealed that these neurons interact with well-known appetite-regulating mechanisms. They are silenced by a hunger-inducing hormone and activated by GLP-1 agonists, a class of drugs used for obesity and diabetes treatment.
“These neurons essentially interpret a broad range of sensory and hormonal signals, ultimately making the decision to stop eating,” Nectow explained.
Implications for Obesity Treatments
Although this study was conducted in mice, the presence of these neurons in the brainstem—a highly conserved region across vertebrates—suggests that humans likely possess similar cells. This finding offers a promising new target for obesity treatments by directly influencing the neural mechanisms that regulate meal termination.
“We believe this is a significant step forward in understanding satiety and how it can be leveraged to combat overeating and obesity,” said Nectow. “Our hope is that these findings will contribute to new therapeutic strategies in the near future.”
The study has been published in the journal Cell.
Disclaimer: This article is for informational purposes only and does not constitute medical advice. While the findings are promising, further research is needed to confirm their application in humans. Always consult a healthcare professional before making any changes to your diet or treatment plans.
