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In a nutshell
- Scientists discovered that the brain cells (POMC neurons) responsible for making us feel full are simultaneously triggering sugar cravings, explaining why we often have room for dessert even after a big meal.
- This sugar-craving mechanism appears to be hardwired into our brains and is specific to sugar; it doesn’t affect our desire for other types of food like fats.
- The finding was confirmed in both mouse studies and human brain scans, suggesting this is a universal trait that could lead to new treatments for managing sugar consumption.
COLOGNE, Germany — Ever wonder why there’s always room for dessert, even after a filling meal? Scientists have discovered that the same brain cells that tell us we’re full are also responsible for making us crave sugary treats. This surprising finding reveals a previously unknown neural circuit that explains why we reach for that slice of cake even when we’re satisfied.
Researchers at the Max Planck Institute for Metabolism Research in Cologne, Germany, led by Dr. Henning Fenselau, have identified a remarkable duality in specialized brain cells called POMC neurons. These neurons have long been known as appetite suppressors, releasing chemicals that signal fullness. However, their new research, published in Science, shows these same cells simultaneously trigger a specific craving for sugar through a different mechanism.
Inside our brains lies a complex network of circuits controlling hunger and satisfaction. POMC neurons, located in a region called the arcuate nucleus, act as central players in this network. When we’re full, these neurons typically release chemicals that reduce our desire to eat. But the research team discovered these neurons have a secret second function: they also release beta-endorphins – natural opioids that can drive sugar consumption.
This dual nature explains a common experience: finishing a satisfying meal only to find yourself eyeing the dessert menu moments later. It’s not just a lack of willpower – your brain is actively pushing you toward that sweet treat, even as it signals that you’ve had enough to eat.
The scientists conducted their investigation using a combination of sophisticated techniques. They employed genetic tools to manipulate specific neurons in mice, allowing them to control these cells with light (optogenetics) and measure their activity in real-time. They also used advanced imaging techniques to watch these neurons in action as mice encountered different foods.
Most intriguingly, when researchers blocked the action of these neurons, mice showed less interest in sugary foods after meals. However, this intervention didn’t affect their consumption of fatty foods, suggesting this circuit is specifically tuned to sugar cravings.
“From an evolutionary perspective, this makes sense: sugar is rare in nature, but provides quick energy. The brain is programmed to control the intake of sugar whenever it is available,” Fenselau says in a statement.
The research extended beyond animal studies. Working with human brain tissue samples, the team confirmed that similar neural circuits exist in human brains. They also conducted brain imaging studies with 30 healthy participants, observing how their brains responded to consuming sugar solutions versus water. The results showed that sugar consumption reduced activity in the same brain region identified in the mouse studies, suggesting a shared mechanism across species.
This discovery could lead to useful therapies for overeating, especially when it comes to sugar. It might explain why desserts have become such a universal cultural phenomenon – our brains are literally wired to want them, regardless of how full we feel.
“There are already drugs that block opiate receptors in the brain, but the weight loss is less than with appetite-suppressant injections. We believe that a combination with them or with other therapies could be very useful. However, we need to investigate this further,” says Fenselau.
Even as your brain tells you you’re full, it’s simultaneously preparing you for dessert. Perhaps that’s why we’ve historically separated our sweets to the end of the meal – our brains were ahead of our cultural practices all along.
Paper Summary
Methodology
The research team used multiple complementary approaches to build their case. They started with detailed mapping of neural circuits in mice, using fluorescent markers to track specific types of neurons and their connections. They then employed optogenetics – a technique that allows neurons to be controlled with light – to manipulate these circuits and observe the effects on behavior. For human studies, they used functional magnetic resonance imaging (fMRI) to observe brain activity patterns in response to sugar consumption.
Results
The key finding was that POMC neurons serve a dual function: they simultaneously signal fullness while triggering sugar cravings through separate mechanisms. When mice were already full, activating these neurons specifically increased their consumption of sugary foods but not fatty foods. In humans, sugar consumption led to decreased activity in the paraventricular thalamus, consistent with the proposed mechanism.
Limitations
While the research provides compelling evidence for this neural circuit in both mice and humans, the human component of the study was limited to brain imaging and tissue analysis. Additional research would be needed to confirm if blocking this circuit could safely reduce sugar cravings in humans. The study also focused primarily on immediate responses to sugar, leaving questions about long-term effects unanswered.
Discussion and Takeaways
This research provides the first biological explanation for why we crave desserts even when full. It suggests that this isn’t simply a matter of habit or lack of self-control, but rather a hardwired neural mechanism that may have evolved when sugar was scarce and valuable as an energy source. Understanding this circuit could lead to new approaches for treating overeating behaviors, particularly those involving sugar.
Funding and Disclosures
The research was supported by multiple organizations including the European Research Council, Deutsche Forschungsgemeinschaft, and various research institutions. Two of the study authors were employees of Novo Nordisk and minor shareholders in the company.
Publication Information
Published in Science, Volume 387, pages 750-758 (2025). The paper titled “Thalamic opioids from POMC satiety neurons switch on sugar appetite” was authored by Marielle Minère and colleagues from the Max Planck Institute for Metabolism Research and several other international institutions.
