A recent study published in Science has shed light on a puzzling phenomenon known as “dessert stomach,” where individuals experience an intense desire for sweet, high-sugar-containing foods even when they feel full after a meal. Researchers at the Max Planck Institute for Metabolism Research discovered that a specific type of neuron, pro-opiomelanocortin (POMC) neurons, plays a key role in this selective appetite for sugar.
The study involved mice and human volunteers who were given access to either regular chow or high-sugar-containing diet for a short period. The researchers found that the mice consumed significantly more calories from the high-sugar diet than from the regular food, even when they were already full. Brain scans revealed that POMC neurons became active as soon as the mice were given access to sugar, triggering an appetite for sweet treats.
The findings suggest that POMC neurons not only promote feelings of satiety but also switch on sugar appetite, driving overconsumption. When the researchers blocked this pathway in the brain, the mice refrained from eating additional sugar. The study’s lead author, Henning Fenselau, believes that understanding this mechanism could lead to new treatments for obesity.
The research group proposes a model where POMC neuron activation triggers two opposing processes: one that decreases food intake through satiety-promoting neurons and another that stimulates sugar intake by inhibiting neurons in the paraventricular nucleus of the thalamus. This finding has implications for our understanding of evolutionary pressures on the brain’s control over sugar intake.
The study’s results may also pave the way for combining existing obesity treatments with new therapies targeting endogenous opioid signaling in sugar appetite regulation. Further research is needed to explore the potential benefits of this approach.
Source: https://www.genengnews.com/topics/translational-medicine/neurons-that-signal-satiety-also-trigger-a-sweet-tooth-in-mice