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Researchers from the University of Maryland and the University of Concepción discovered that the satiety signal in the brain depends on astrocytes, cells previously seen only as support, that receive lactate from tanycytes after a meal and activate neurons that send stop eating signals, paving the way for new treatments against obesity.
For years, science believed that the decision to stop eating depended almost exclusively on neurons, the most well-known signaling cells in the brain. But a study published in the Proceedings of the National Academy of Sciences in April 2026 revealed that the brain uses a much more complex system, involving cells that researchers considered mere supporting actors. Astrocytes, previously classified as support cells for neurons, play an active role in regulating appetite and are the missing piece to understand why some people simply cannot feel full.
The discovery was made by researchers from the University of Concepción in Chile, in collaboration with the University of Maryland. They identified a previously unknown signaling pathway in the hypothalamus, the region of the brain that controls hunger and satiety. “People tend to think immediately of neurons when they think about how the brain works,” explained Ricardo Araneda, a biology professor at the University of Maryland. “But we are discovering that astrocytes also participate in how our brain regulates the amount of food we consume. This research changes the way we think about these communication circuits.”
How the brain detects that you have eaten enough
The process begins with specialized cells called tanycytes, which line a fluid-filled cavity inside the brain and monitor glucose levels in the cerebrospinal fluid.
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After a meal, blood glucose levels rise, and tanycytes respond by processing this sugar and releasing lactate, a metabolic byproduct, into the nearby brain tissue. Until now, scientists believed that this lactate communicated directly with the neurons responsible for appetite control.
But the team discovered that there is an unexpected intermediary in this communication: the astrocytes in the brain. Astrocytes have a receptor called HCAR1 that detects lactate. When lactate binds to this receptor, astrocytes are activated and release glutamate, a chemical messenger that is then transmitted to the neurons that suppress appetite.
The result is the feeling of fullness. In other words, the “stop eating” signal in the brain travels through a chain that goes from blood sugar, passes through tanycytes, reaches astrocytes, and only then reaches the neurons.
The chain reaction that spreads through the brain after each meal
In one of the most revealing experiments of the study, scientists introduced glucose into a single tanycyte while observing the nearby astrocytes in the brain.
Even this localized change triggered activity in multiple neighboring astrocytes, showing how the fullness signal can propagate in a chain through the brain network from a single point. The system works like a cascade of biological dominoes.
The researchers also noted a dual effect in the brain. The hypothalamus contains two opposing populations of neurons: those that promote hunger and those that suppress it.
Lactate appears to act on both simultaneously, activating the satiety neurons through the astrocytes and potentially calming the hunger neurons through a more direct pathway. “What surprised us was the complexity of this,” said Araneda. “In simple terms, we found that tanycytes ‘talk’ to astrocytes, and astrocytes ‘talk’ to neurons.”
Why this discovery in the brain could change obesity treatment
The newly discovered signaling pathway opens up a completely new perspective for medical science. If the astrocytes in the brain function as essential intermediaries in appetite control, any dysfunction at this stage could explain why some people do not receive the satiety signal even after sufficient meals.
In people with obesity, this communication chain may be compromised at a point that current treatments do not reach.
“Now we have a different mechanism that allows us to target astrocytes or, specifically, the HCAR1 receptor in the brain,” emphasized Araneda. “It would be a new target that could complement existing therapies like Ozempic, for example, and improve the lives of many people suffering from obesity and other appetite-related disorders.”
Currently, there are no medications that directly act on this pathway, but the discovery signals a promising direction for the development of new therapies.
The role of astrocytes that brain science has ignored for decades
Astrocytes are among the most common types of cells in the brain and are named for their star-like shape. For decades, science treated them as passive infrastructure that merely nourished and protected neurons, without direct involvement in the decisions of the nervous system.
The study published in the Proceedings of the National Academy of Sciences challenges this view by demonstrating that, in appetite control, astrocytes are not mere bystanders. They are protagonists in a stage without which the satiety signal simply would not reach the neurons.
The discovery reflects a growing trend in neuroscience to recognize that the brain operates with more layers of complexity than the neuron-centered model allowed us to understand. Both tanycytes and astrocytes exist in all mammals, including humans, suggesting that the same mechanism identified in animal models may be at work in the human brain.
The next steps for the team include testing whether altering the HCAR1 receptor in astrocytes can influence feeding behavior in more complex models.
What comes next after this discovery about the satiety switch in the brain
The findings are the result of nearly ten years of collaborative work between the laboratories of the University of Maryland and the University of Concepción. The lead author of the study, Sergio López, is a PhD student supervised by both institutions and conducted crucial experiments during an eight-month research visit to UMD.
The research was funded by the National Fund for Scientific and Technological Development of Chile, the Millennium Institute of Neurosciences, and the National Institutes of Health of the USA.
For brain science, the discovery that astrocytes control part of appetite is comparable to discovering that the backstage of a theater influences the script of the play, not just the lighting. Those who always believed that neurons commanded everything now need to include astrocytes in the equation.
And for millions of people struggling with obesity or eating disorders, the possibility that a new therapeutic target in the brain is within the reach of science is the most relevant news this field has produced in years.
What do you think about discovering that the satiety signal in the brain depends on cells that no one thought had this function? Do you believe this discovery could change the treatment of obesity? Share in the comments. Research that changes the way we understand our own body deserves debate, especially when it can affect the lives of millions of people.
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