Insulin receptor signaling in gustatory cells suppresses sugar taste sensitivity and feeding in Drosophila

Abstract

Dynamic sensory processing helps animals adjust behaviors in response to changing environments and internal states. Hunger is a salient internal cue that can directly modify chemosensory signaling to promote homeostatic behavior. In Drosophila melanogaster, hunger enhances the sensitivity of sweet gustatory receptor neurons (GRNs) to encourage feeding, and here we investigated candidate hunger/satiety hormone receptors to identify mechanisms of metabolic regulation in primary taste cells. The conserved insulin receptor (InR) is expressed in sweet GRNs, and targeted InR knockdown and inactivation within these cells elevated sucrose sensitivity, increased sucrose consumption, and altered feeding behavior under sated conditions. Additionally, sweet cellular responses to sucrose were reciprocally affected by inactive and overactive InR signaling. These findings reveal that InR signaling can modulate sweet sensitivity at the level of primary taste cells, suppressing feeding by reducing taste responsiveness under specific metabolic conditions.