The mystery of why we crave dessert, even after a filling meal, has been unraveled by researchers at the Max Planck Institute for Metabolism Research in Cologne. They discovered that specific brain cells (POMC neurons) play a dual role in both signaling fullness and triggering sweet cravings. These neurons release β-endorphin, a natural opiate, when sugar is detected, creating a reward response that encourages sugar consumption even in satiated individuals.
This “dessert stomach” mechanism is activated merely by perceiving sugar and exists in both mice and humans, with brain scans confirming similar neural responses across species. Researchers found this evolutionary adaptation makes sense given sugar’s rarity in nature, and its value as a quick energy source. Therefore, blocking this opiate pathway could potentially aid in treating obesity. All in all, the discovery of this neural mechanism is particularly significant, as it could lead to more effective obesity treatments, possibly through combining existing opiate receptor blockers with other therapeutic approaches.
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