Neuronal GLP1 receptors are required for conditioned taste aversion induced by liraglutide in mice, as genetic deletion of these receptors abolishes the development of flavor aversion paired with liraglutide administration, demonstrating that central GLP1 receptor signaling mediates this nausea-like behavioral response.

Liraglutide enters the brain and binds to specific receptors on certain nerve cells in a region that controls hunger. This binding directly activates those nerve cells and triggers signals that suppress appetite and create a feeling of sickness. When the drug is paired with a specific taste, the brain links that taste to the sickness, causing the animal to avoid it in the future.