Brain Cells in Mice Unveil Secrets of Human Eating Speed and Appetite Regulation

According to research done at the University of California, San Francisco, specific brain cells are responsible for both eating behavior and the ability to quit feeding in mice. These ground-breaking discoveries, published in Nature, opened up new avenues for researchers interested in understanding how humans manage their food consumption. 

In mice, vagal nerves in the colon have been demonstrated to play an essential role in controlling food intake and choice. In both mice and humans, the caudal nucleus of the solitary tract in the brainstem is linked to controlling decreased food consumption. This area contains two types of neurons: those that release prolactin (PRLH) and those that secrete glucocorticoids (GCG). 

Previous experiments depended on sedating mice and feeding them liquid meals, raising concerns about the active status of the neurons. In an effort to address this information gap, neuroscientist Zachary Knight and his team placed light sensors into the brains of genetically engineered mice. PRLH neurons are engineered to release a fluorescent signal when stimulated by nerve impulses from elsewhere in the body. 

Scientists administered Ensure, a liquid diet high in fat, protein, sugar, vitamins, and minerals, straight into the stomachs of these mice. PRLH neuron activity increased during feeding and peaked shortly after the infusions were stopped. The neurons’ inactivity when a saline solution was substituted for the liquid meal demonstrates that they are susceptible to nutritional levels. 

When mice were given unrestricted access to liquid food, the PRLH neurons were active during licking and then quieted down when the animals stopped. This result adds to our understanding of appetite control by implying that oral cues are more essential than digestive ones. 

Laser activation of PRLH neurons resulted in a significant decrease in food intake in freely-fed mice, according to researchers. More research demonstrated that a sweet taste was necessary to activate PRLH neurons. Furthermore, GCG neurons were discovered to be triggered by stomach signals, controlling the end of eating. 

Harvard University neuroscientist Chen Ran praised the study for its “novel insights” into the relationship between flavor and hunger. Because the same neural pathways identified in mice are likely to exist in humans, these findings could help explain how humans regulate their appetite. 

The study’s results have far-reaching ramifications because they pave the door for further research into the complicated brain networks that govern human hunger. This discovery provides insight into the intricate ways in which brain cells collaborate to define our connection with food and might lead to novel therapies for disorders such as appetite dysregulation. 

Journal Reference  

Wong, C. (2023). These brain cells could influence how fast you eat – and when you stop. Retrieved from https://www.nature.com/articles/d41586-023-03679-y