Nociception is one of the most important physiological functions. Interestingly, external factors such as weather and nutrient affect nociception in mammals. Thus, the nociceptive system can be modified in response to environmental conditions. In many species, feeding is essential for life and hunger also induces the modification of physiological functions. In this study, we examined whether starvation affects heat nociception using the fruitfly, Drosophila melanogaster. It is an excellent model organism to identify genes and genetic pathways important for nociception, because it shows behavioral avoidance of noxious heat like mammals and vast genetic information and tools are available. When wild-type (WT) adults are placed on a hot plate (> 45°C), they show robust jumping behavior. This behavior can be used as a measure of noxious heat responses. 12h starvation caused reduction of heat responses in comparison with non-starved flies. However, 6h or 18h starvation did not affect. Next, we examined whether headless flies also show the starvation-inducible phenotype in heat nociception. Headless flies are known to retain a variety of functional sensory inputs and we previously reported that they show a brain-independent noxious heat response (tumbling). When flies were decapitated after 12h starvation, their heat nociception was not modified, suggesting that starvation-inducible reduction of heat responses results from the modification of physiological states of the brain. In Drosophila, hunger and satiety are regulated by neuropeptides released from neurosecretory cells in the brain. Thus, we next focused on three neuropeptide receptors [Insulin receptor (InR), leukokinin receptor (Lkr) which is thought to be homologous to vertebrate tachykinin receptors, and neuropeptide F receptor (NPFR)], which are involved in the regulation of feeding behavior, and measured heat nociception of their mutants without starvation. In comparison with WT flies, heat nociception of InR mutant was enhanced, while that of Lkr mutant was reduced. Furthermore, leukokinin mutant also showed Lkr-like phenotype. Taken together, it seems likely that leukokinin signaling is involved in starvation-inducible reduction of heat nociception in Drosophila.