Researchers at the Max Planck Institute for Metabolism Research have found that our brain’s “opiate pathway” plays a key role in why we crave sweets even when full. The study, published in Science journal, reveals that the same nerve cells responsible for feeling full after a meal are also triggered by sugar.
The researchers investigated mice and discovered that completely satiated animals still ate desserts. Brain scans showed that specific nerve cells called POMC neurons became active when mice were given access to sugar, releasing signaling molecules that stimulate appetite and one of the body’s own opiate: ß-endorphin. This triggers a feeling of reward, causing mice to consume more sugar beyond fullness.
Interestingly, this mechanism was already activated before the mice ate sugar, and the release of ß-endorphin was observed even in mice that had never eaten sugar before. Brain scans on human volunteers who received a sugar solution showed similar results, suggesting that the brain’s response to sugar is similar across species.
According to Henning Fenselau, research group leader, this finding makes sense from an evolutionary perspective: sugar provides quick energy and our brains are programmed to control its intake. The study suggests that blocking opiate receptors in the brain could be useful for treating obesity, but further investigation is needed.
The discovery has significant implications for understanding why we crave sweets even when full, and could lead to new treatments for obesity and related disorders.
Source: https://medicalxpress.com/news/2025-02-brain-opiate-pathway-crave-sweets.html