In a new study, researchers led by the Max Planck Institute for Metabolism Research have unearthed a scientific explanation for the ubiquitous phenomenon known as the "dessert stomach." Their findings, recently published in the journal Science, shed light on why we continue to crave sweets even when we're completely satiated -- a breakthrough that could also hold significant implications for obesity treatment.
The researchers investigated the response of mice to sugar, discovering that even when these mice were fully satisfied with regular food, they still consumed dessert-like sugary treats. Key to this behavior is a specific group of neurons in the brain, known as POMC neurons. These neurons become active upon sugar intake, irrespective of the mice's satiation level.
When mice that were already full consumed sugar, their POMC neurons released signaling molecules indicating satiety. Remarkably, these neurons also emitted one of the body's natural opioids: ß-endorphin. Through its interaction with other neurons having opiate receptors, this opioid created a rewarding sensation, prompting the mice to eat sugar beyond their fullness.
Interestingly, this opioid pathway was uniquely triggered by sugar intake, but not by consumption of normal or fatty foods. However, when the researchers blocked this pathway, the overindulgence in sugar ceased, though this effect was exclusively seen in full mice. Hungry mice showed no difference with the inhibition of ß-endorphin release.
Further intrigue arose as this neural mechanism activated not just upon consuming sugar, but also upon the sensory perception of it. Even mice that had never encountered sugar before exhibited a release of ß-endorphin upon their first taste.
To bridge this animal model with human behavior, the researchers conducted brain scans on volunteers given a sugar solution. The same brain region showed a similar reaction to sugar in humans, housing numerous opiate receptors near neurons that regulate satiety.
The researchers assert that this behavior is evolutionarily advantageous.
"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," Henning Fenselau, research group leader at the Max Planck Institute for Metabolism Research and head of the study, said in a news release.
The implications of this discovery extend beyond mere curiosities of human behavior; they may influence future treatments for obesity.
"There are already drugs that block opiate receptors in the brain, but the weight loss is less than with appetite-suppressant injections," Fenselau added. "We believe that a combination with them or with other therapies could be very useful. However, we need to investigate this further."
This study not only highlights a fascinating aspect of human appetite but also underscores the complexity of our brain's interaction with food, potentially paving the way for innovative obesity treatments.
By understanding the brain's "dessert stomach," we might be able to devise strategies that mitigate our seemingly insatiable craving for sugar, aligning our modern dietary habits more closely with our evolutionary biology.