Research Reveals How the Brain Regulates Food Consumption

Scientists at Columbia University’s Zuckerman Institute have identified a brain region in mice that can amplify or repress the drive to consume not only sweets but also salt, fat, and food. Their study explored why people crave sugar and other energy-dense foods when tired and sought to clarify the link between appetite stimulation and consumption. The research details how a brain “dial,” located in the bed nucleus of the stria terminalis (BNST), controls various consummatory behaviors by integrating internal needs with sensory cues.

The team began by focusing on the amygdala, the brain’s emotion center known for processing pleasure and discomfort. They found specific neurons within the central amygdala that respond to sweet tastes. Each neuron possessed branches connecting to the BNST, a region previously linked to feeding and reward responses. By selectively stimulating BNST-associated neurons, researchers caused mice that had already eaten to continue consuming sweets. Suppressing these neurons led very hungry animals to eat less, showing the importance of this circuit in modulating food intake.

Further experiments demonstrated that this brain area does not limit its control to sweets. The BNST also influences mice’s urge to consume salt, fat, and general food, suggesting broader control over eating behavior. Anatomical studies revealed connections between the BNST and other brain regions that help sense an animal’s internal states, such as hunger or the need for salt. "We now have a better understanding of how the brain integrates specific internal needs with sensory signals in order to elicit appropriate consummatory responses," said José A. Cánovas, first author of the paper published in Cell. 

The implications extend to clinical concerns like cachexia, a severe appetite loss and weight decline commonly seen in chemotherapy patients. When researchers gave mice a chemotherapy drug known to cause cachexia-like symptoms, stimulating the BNST helped protect them from weight loss. "Maybe stimulating this brain area can help address this issue," noted Li Wang, the study’s co-lead author. Conversely, inhibiting the BNST triggered marked weight loss in mice. The team also discovered that the weight-loss drug semaglutide (Ozempic, Wegovy) targets BNST neurons. "Perhaps a better understanding of the BNST may lead to therapies that help suppress consumption without these effects," added Dr. Cánovas. 

This study indicates that modulating the BNST could offer precision approaches to treating both overeating and loss of appetite by adjusting the brain’s consumption “dial.”