CENTER FOR NEUROMETABOLISM

Published in Nature Metabolism, this study reveals how GLP-1—the same hormone targeted by widely used weight-loss drugs such as Ozempic—acts in the brain to regulate food intake. Researchers at the CNM identified a specific neural circuit connecting the hypothalamus and brainstem that is strengthened by GLP-1 signaling and, when activated, suppresses feeding. Notably, this circuit dynamically adapts to internal state, responding more strongly to GLP-1 during hunger than satiety. In obesity, however, this flexibility is impaired, providing new insight into how GLP-1–based therapies act on the brain and why their effects may vary across metabolic states.

Published in Nature Communications, researchers at the CNM identified a neural circuit linking the extended amygdala to the lateral hypothalamus that adjusts reward-seeking behavior based on energy state. The pathway becomes more active during hunger, increasing motivation for food, and less responsive during satiety. This circuit shows dynamic plasticity, tuning behavior to match metabolic needs. Disruption of this plasticity may contribute to overeating and broader disorders involving reward and motivation.

In the News: Two Rutgers Teams Trace Brain Circuits That Tell Us When to Eat – and When to Stop

Published in Molecular Metabolism, researchers at the center show that GLP-1 receptor–expressing neurons in the dorsolateral septum project to the lateral hypothalamus, forming an inhibitory circuit that suppresses food intake. Manipulating this pathway directly alters feeding behavior. This study highlights a previously underappreciated brain pathway and identifies new potential targets for treating obesity and eating disorders. 

Published in Bioscience Reports, this study reveals that viral vector–mediated toxicity in the paraventricular hypothalamic nucleus (PVN) can lead to significant metabolic and behavioral disturbances. The researchers at the CNM show that unintended neuronal damage in this key regulatory hub disrupts energy balance and alters feeding-related behaviors. These findings highlight an important technical and biological consideration when using viral tools to manipulate hypothalamic circuits.

Published in Molecular Metabolism, researchers at the CNM reveal that maternal overnutrition rewires feeding circuits in the developing brain. By altering synaptic input to the lateral hypothalamic area, early-life nutritional excess programs long-term changes in energy balance and increases susceptibility to obesity.