You swear you could not eat another bite. However, when the dessert arrives, your craving kicks in and you suddenly have an appetite for something sweet. This phenomenon, popularly called the “dessert stomach,” is more than a habit or indulgence. Researchers from the Max Planck Institute for Metabolism Research have discovered that our brains are wired to crave sugar even when we are full due to a specific neural pathway that overrides satiety signals and activates our reward system.
Having Room For Dessert: Nerve Cells that Signals Satiety Also Signals Sugar Cravings
A series of experiments by M. Minère et al. studied mouse brains and confirmed their findings using human brain scans. Their purpose was to understand the neurobiological mechanisms that drive overeating by focusing on the sensory-specific satiety phenomenon in which people feel full from a meal but still crave foods with different tastes. Their findings, which were published on 13 February 2025 in Science, revealed a specific neural pathway that regulates the drive for sweet foods in a state of satiety.
Results from Mice and Humans
The researchers conducted a series of experiments on mice and humans that combined behavioral analysis, neuroimaging, and neural pathway manipulation. Take note of the following:
• Mouse Observation: Researchers observed whether satiated mice would continue consuming sugar when given access. They compared sugar consumption to other types of food like normal and fatty food to see if the response was sugar-specific. Mice continued to consume sugar even when full. This suggested an override of satiety signals.
• Identification of Specific Neurons: Brain activity was monitored to identify which neurons were activated when sugar was consumed. They found that pro-opiomelanocortin or POMC neurons in the hypothalamus, which usually promote satiety, also triggered sugar cravings. These neurons sent signals to the paraventricular thalamus. Take note that this region in the brain is involved in pleasure and motivation.
• Role of Opioid Signaling: Sugar consumption activated mu-opioid receptors, releasing β-endorphin, a natural opiate that enhances pleasure and reward. These opioid receptors were blocked to confirm its link with sugar cravings. Satiated mice stopped overeating sugar upon blocking. Hungry mice were unaffected. This indicated that the opioid pathway specifically drives sugar cravings beyond normal hunger.
• Human Brain Scans: Researchers confirmed its relevance to humans by conducting brain scans on volunteers who received sugar solutions. The scans showed that the same brain region activated in mice also lit up in humans. This result also supported the idea that sugar cravings after satiety are driven by an evolutionary reward mechanism.
Implications and Further Takeaways
“From an evolutionary perspective, this makes sense. Sugar is rare in nature, but provides quick energy.” Explains Henning Fenselau, research group leader at the Max Planck Institute for Metabolism Research and head of the study. “The brain is programmed to control the intake of sugar whenever it is available.”
The study reveals that sugar cravings in a state of satiety are not just a matter of habit or preference but are actively driven by a neural mechanism involving POMC neurons and opioid signaling. This insight could help in developing targeted treatments for sugar overconsumption and obesity by disrupting the specific neural circuits responsible for excessive sugar intake.
Researcher S. Farooqi underscored the broader context and significance of the study. He noted that their findings improve our understanding of how the brain overrides fullness signals to drive sugar cravings. These are critical not only in understanding but also in addressing people with overeating tendencies and problems.
FURTHER READINGS AND REFERENCES
- Farooqi, S. 2025. “Understanding the Desire for Dessert. In Science. 387(6735): 717-718. American Association for the Advancement of Science. DOI: 1126/science.adv4359h
- Minère, M., Wilhelms, H., Kuzmanovic, B., Lundh, S., Fusca, D., Claßen, A., Shtiglitz, S., Prilutski, Y., Talpir, I., Tian, L., Kieffer, B., Davis, J., Kloppenburg, P., Tittgemeyer, M., Livneh, Y., and Fenselau, H. 2025. “Thalamic Opioids from POMC Satiety Neurons Switch on Sugar Appetite. In Science. 387(6735): 750-758. American Association for the Advancement of Science. DOI: 1126/science.adp1510