Nerve cells that tell to us we are full also make us crave sweets
Who hasn't been there? The big meal is over, you're full, but the craving for sweets remains. Researchers from the Max Planck Institute for Metabolism Research in Cologne have now discovered that what we call the "dessert stomach" is rooted in the brain. The same nerve cells that make us feel full after a meal are also responsible for our craving for sweets afterwards. In mice and humans, the "dessert-stomach pathway" is activated by mere perception by releasing the opiate ß-endorphin, which makes evolutionary sense because sugar provides quick energy. Blocking opiate signaling of this pathway may support current and future obesity treatments.
Our brain has a sweet tooth.
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To find the cause of the "dessert stomach", the researchers investigated the reaction of mice to sugar and found that completely satiated mice still ate desserts. Investigations of the brain showed that a group of nerve cells, the so-called POMC neurones, are responsible for this. These neurones become active as soon as the mice were given access to sugar which facilitated their appetite.
When mice are full and eat sugar, these nerve cells not only release signaling molecues that stimulate satiety, but also one of the body's own opiate: 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.
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.
