Nerve cells that signal when we are full also trigger cravings for sweets.
Most people have experienced this: you’ve finished a big meal, you’re full, yet you still crave something sweet. Researchers at the Max Planck Institute for Metabolism Research in Cologne have discovered that this “dessert stomach” phenomenon is driven by the brain. The same nerve cells responsible for signaling fullness after a meal also play a role in triggering a craving for sweets. In both mice and humans, simply perceiving dessert activates this pathway, releasing the opiate ß-endorphin. This makes evolutionary sense, as sugar provides a rapid energy boost. Blocking opiate signaling in this pathway could support current and future obesity treatments.
To investigate the underlying cause, researchers studied mice and found that even when fully satiated, they continued to consume sugary foods. Brain analyses revealed that a specific group of nerve cells, known as POMC neurons, were responsible for this response. These neurons became active as soon as the mice were exposed to sugar, enhancing their appetite despite prior fullness.
When mice are full and eat sugar, these nerve cells not only release signaling molecules that stimulate satiety, but also one of the body’s own opiates: ß-endorphin. This acts on other nerve cells with opiate receptors and triggers a feeling of reward, that causes the mice to eat sugar even beyond fullness. This opioid pathway in the brain was specifically activated when the mice ate additional sugar, but not when they ate normal or fatty food. When the researchers blocked this pathway, the mice refrained from eating additional sugar. This effect was only observed in full animals. In hungry mice, the inhibition of ß-endorphin release had no effect.
Interestingly, this mechanism was already activated when the mice perceived the sugar before eating it. In addition, the opiate was also released in the brains of mice that had never eaten sugar before. As soon as the first sugar solution entered the mice’s mouths, ß-endorphin was released in the “dessert stomach region”, which was further strengthened by additional sugar consumption.
What happens in humans?
The scientists also carried out brain scans on volunteers who received a sugar solution through a tube. They found that the same region of the brain reacted to the sugar in humans. In this region, as in mice, there are many opiate receptors close to satiety neurons.
“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,” explains Henning Fenselau, research group leader at the Max Planck Institute for Metabolism Research and head of the study.
Relevance for the treatment of obesity
The research group’s findings could also be important for the treatment of obesity.
“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.
Reference: “Thalamic opioids from POMC satiety neurons switch on sugar appetite” by Marielle Minère, Hannah Wilhelms, Bojana Kuzmanovic, Sofia Lundh, Debora Fusca, Alina Claßen, Stav Shtiglitz, Yael Prilutski, Itay Talpir, Lin Tian, Brigitte Kieffer, Jon Davis, Peter Kloppenburg, Marc Tittgemeyer, Yoav Livneh and Henning Fenselau, 13 February 2025, Science.
DOI: 10.1126/science.adp1510
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