Characterization and postprandial regulation of the nutrient-sensing machinery in the oral floor mucosa of 10-week-old mule ducks.

In birds, oral nutrient detection contributes to regulating ingestive behavior, yet the molecular repertoire and postprandial dynamics of gustatory pathways remain poorly defined in ten-week-old ducks. This study evaluated the postprandial responses of nutrient-sensing receptors, calcium-signaling components, and monoaminergic pathways in the oral floor mucosa and central neural tissue of ten-week-old mule ducks. Fed and fasted ducks were sampled at 0 min, 20 min, 2 h, 6 h, and 12 h following meal distribution. Transcriptional profiling revealed a broad chemosensory repertoire spanning sweet, umami, bitter, sour, and fatty acid modalities in the oral floor mucosa, supporting its role as a key sensory interface. However, most gustatory and calcium-signaling genes exhibited remarkable transcriptional stability postprandially at this developmental stage. Notably, only the lipid sensor CD36 (Cluster of differentiation 36) and the bitter receptor T2R116 (Taste receptor type 2 member 116) displayed a significant time × feeding interaction, indicating targeted peripheral responsiveness for fat and bitter perception. Conversely, postprandial changes were marked in monoaminergic circuits. Serotonin metabolism in the oral floor mucosa varied by nutritional state during the early postprandial phase, while elevated central serotonin concentrations and enhanced dopaminergic turnover in fed ducks evidenced acute activation of central satiety and reward circuits. Concurrently, hypothalamic gene expression revealed a synchronized time-dependent downregulation of POMC (Proopiomelanocortin) and MC4R (Melanocortin 4 receptor) up to 6 h post-feeding. In parallel, plasma chemerin levels increased postprandially, highlighting a coordinated peripheral metabolic response. Overall, these results indicate that short-term postprandial regulation in ten-week-old ducks relies predominantly on rapid neurochemical adjustments rather than transcriptional remodeling of peripheral gustatory receptors.