Brain Circuits & Appetite: Eat vs. Stop Signals
- Two new studies from Rutgers Health reveal the intricate communication between the stomach and brain, highlighting a complex interplay of signals that either stimulate or suppress appetite.
- One study, lead by Zhiping Pang at Robert Wood Johnson Medical School, focused on a specific group of neurons connecting the hypothalamus and brainstem.
- Mark Rossi, co-leader of the Center for NeuroMetabolism, led the second study, which mapped the hunger-triggering circuit.
New research unveils critical brain circuits controlling hunger and satiety, potentially revolutionizing weight loss. Rutgers Health studies illuminate pathways that either stimulate or suppress appetite, offering key insights for more effective medications with fewer side effects. Scientists have identified specific neurons and the hormones that govern our eating behaviors, including those targeted by drugs like Ozempic. The findings demonstrate that some brain circuits act as the accelerator for hunger,while others function as the brake. This vital research, which News Directory 3 is reporting on, may lead to the growth of next-generation weight-loss drugs. Discover what’s next in the battle against obesity.
Brain Circuits Unveiled: New Targets for Weight Loss Drugs
Updated June 10, 2025
Two new studies from Rutgers Health reveal the intricate communication between the stomach and brain, highlighting a complex interplay of signals that either stimulate or suppress appetite. These findings, published in Nature Metabolism and Nature Communications, offer a detailed map of hunger and satiety pathways, potentially leading to more effective weight-loss medications with fewer side effects.
One study, lead by Zhiping Pang at Robert Wood Johnson Medical School, focused on a specific group of neurons connecting the hypothalamus and brainstem. These cells are rich in GLP-1 receptors, the same proteins targeted by drugs like Ozempic. The research showed that stimulating this pathway in mice led to decreased eating, while silencing it caused weight gain. pang noted that the connection strengthens when energy stores are low, suggesting that constant stimulation from drugs could disrupt the brain’s natural rhythm and cause side effects.
Mark Rossi, co-leader of the Center for NeuroMetabolism, led the second study, which mapped the hunger-triggering circuit. His team identified inhibitory neurons in the stria terminalis that connect to similar cells in the lateral hypothalamus. Activating this connection prompted hungry mice to seek sugar water, while blocking it reduced their appetite even after fasting. The effect was modulated by hormones: ghrelin increased food-seeking behavior, while leptin suppressed it. Overfed mice initially lost this response, but it returned after weight loss.
Rossi explained that while Pang’s pathway acts as a “shut-down” mechanism, his pathway “steps on the accelerator” for hunger. Both teams observed that energy state rapidly rewires synapses. Fasting increases the hunger circuit’s sensitivity while decreasing the satiety circuit’s effectiveness, and the opposite occurs after eating.
This research marks the first observation of this push-pull mechanism operating in parallel pathways. This ”yin-yang” arrangement may explain why treatments targeting only one side of the equation lose effectiveness over time. It also suggests possibilities for developing drugs that surpass the current generation of GLP-1 medications in efficacy and tolerability.
The scientists suggest that future therapies could target only the brain