'Brain Dial' Discovered in Mice That Regulates Food, Fat, and Salt Cravings

Researchers at Columbia University's Zuckerman Institute have identified a specific brain region in mice that functions as a 'dial' to control the desire to consume various substances, including sweets, fats, and salt. This discovery sheds light on how the brain orchestrates feeding behavior and internal needs.

The study reveals that this brain area can either amplify or suppress the motivation to eat, offering a new understanding of the neural mechanisms behind appetite regulation. The researchers found that stimulating neurons in this region, known as the bed nucleus of the stria terminalis (BNST), could prompt fully fed mice to continue consuming sweets. Conversely, inhibiting these neurons significantly reduced their desire to eat, even when they were hungry.

The team first examined the amygdala, a brain center involved in emotions and reward processing, discovering neurons there that respond to sweetness. These neurons extend connections to the BNST, which plays a role in feeding behavior. When neurons linked to the BNST were stimulated, mice that had already eaten their fill resumed consuming sweets. Suppressing activity in the BNST had the opposite effect, diminishing appetite.

Beyond sweets, the BNST was found to influence craving for salt, fats, and general food intake, indicating its role as a centralized 'regulator' of consumption. Anatomical links between the BNST and brain circuits monitoring internal states, like hunger and salt deficiency, support its integrative function.

This research has promising implications for medical treatments. For example, in chemotherapy patients experiencing cachexia—a condition involving severe weight and appetite loss—targeting this brain circuit might help restore appetite. Additionally, inhibiting the BNST could be a strategy for weight loss, as its suppression led to significant weight reduction in mice.

Interestingly, the study also found that the weight-loss drug semaglutide targets neurons within the BNST, providing insight into how it might suppress appetite. However, the drug's side effects, such as nausea, suggest that future therapies could benefit from a more precise approach directly targeting the BNST.

The findings, published in illment in ell in Cell, open new pathways for developing therapies aimed at controlling excessive or insufficient eating behaviors. Dr. Charles S. Zuker emphasized that this work identifies a central brain region that coordinates feeding responses, potentially revolutionizing treatments for eating disorders and cachexia.

More information about this research can be found in the original publication: DOI: 10.1016/j.cell.2025.08.021.