Ever finished a big meal, feeling completely full, yet finding yourself craving for something sweet? This common phenomenon many of us might have experienced has a scientific explanation.
Researchers at the Max Planck Institute for Metabolism Research have uncovered how the brain drives this irresistible urge for sugar, even when the body has had enough food.
Even after sending the satiety signal, the same nerve cells may have a part in triggering a craving for sweets. The study says that in both mice and humans, even the prospect of having a dessert activates this pathway, releasing the opiate ß-endorphin.
Beta-endorphin (β-END) is a naturally occurring opioid peptide that is produced in the brain and pituitary gland. It has many effects in the body, including pain relief, reward behavior, and homeostasis.
Having a dessert after a heavy-calorie meal would of course lead to fat accumulation and unwanted weight gain. Blocking opiate signaling in this pathway could support current and future obesity treatments.
Why do we crave sugary snacks on full stomach?
To find out more about the brain’s unique mechanism, researchers conducted experiments on mice and decoded why sugary snacks are so enticing even on a full stomach.
The mice involved in the analyses continued to crave sugary foods even when fully satiated. The analysis of their brain revealed that a particular group of nerve cells, known as POMC neurons, triggered this response. The neurons tended to become active as soon as the mice were exposed to sugar, enhancing their appetite despite feeling full.
A unique pathway that triggers feelings of reward in the brain was activated when sweet treats were consumed by the mice.
When mice are full and consume sugar, their nerve cells release not only satiety-signaling molecules but also ß-endorphin, a natural opiate. When it interacts with opiate receptors in the brain, it creates a sense of reward that drives the mice to continue eating sugar even when they are already full.
Interestingly, this opioid pathway was specifically activated by sugar consumption, but not by regular or fatty foods. However, when researchers blocked this pathway, the mice stopped eating extra sugar—though this effect only occurred in full mice. In hungry mice, preventing ß-endorphin release had no impact on their eating behavior.
This mechanism also came into play when mice perceived the sugar before eating it. The opiate was also released in the brains of mice that had never eaten sugar before. As soon as sugar entered the mice’s mouths, ß-endorphin was released in the ‘dessert stomach region’, which was further strengthened by further sugar consumption.
Does it apply to humans too?
It brought similar results in humans too. When the experiment was carried out on humans and they got sugar solution through the tube, the same region of the brain was activated.
“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.
“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.
