Why we crave dessert even when we are full

Even after eating a large meal, most people can still find room for sweets. Now, research in mice shows that the neurons behind feeling full also trigger sugar cravings. In other words, there seems to be a neurological basis for our love of dessert. (I)
Previous studies have shown that naturally occurring opioids in the brain play a crucial role in sugar cravings. The main producers of these opioids are neurons located in a brain region that regulates appetite, metabolism and hormones. Known as pro-opiomelanocortin (POMC) neurons, they also control feelings of satiety after eating.
To understand whether these cells have a role in sugar cravings, Henning Fenselau at the Max Planck Institute for Metabolism Research in Germany and his colleagues traced the opioid signals that POMC cells send in the brain. They did so by bathing brain slices from three mice in a fluorescent solution that binds to receptors of these opioids. (II) The brain region with the highest density of these receptors was the paraventricular nucleus of the thalamus (PVT), known to regulate feeding. That suggested sugar cravings were related to communication between these two brain regions. This observation provided a clearer map of the neural circuitry involved, allowing the researchers to focus on specific pathways rather than general brain activity. It also helped establish a functional link between receptor density and behavioural outcomes related to food intake, thereby strengthening the overall reliability of their experimental approach. (III)
Subsequently, the researchers monitored the activity of neurons in these regions as mice ate their usual food. When the animals seemed to be full, the team gave them a dessert of sugary chow. (IV) On average, neuronal activity between the brain regions roughly quadrupled while mice ate dessert compared with their regular meal. The spike began prior to eating the sweets, suggesting the pathway dictates sugar cravings. When the team inhibited signals from POMC neurons to the PVT, the mice consumed 40 percent less dessert. “The cell types, which are extremely well-known for driving satiety, also release signals that cause the appetite for sugar, and they do so particularly in the state of satiety,” says Fenselau. “This would explain why animals – humans – over-consume sugar when they’re actually full.” The pathway may have evolved because sugar is more easily turned into energy than other sources like fats or proteins.
(Adapted from New Scientist, issue dated March 22, 2025)