Sleep is regulated by a diversity of processes, such as circadian rhythm, homeostatic rebound, and dietary intake. While these inputs generally affect long-term sleep over hours or days, it is also thought that consuming food can induce an immediate, but transient, rise in sleep. Despite efforts to uncover mechanisms that drive postprandial sleep, little is known about how this behavior is regulated. Here, we developed a system for simultaneously measuring the sleep and food intake of individual Drosophila and found that animals experience a transient rise in sleep following meals. The effect of ingestion ranged from slightly arousing to strongly sleep inducing, depending on the amount of food consumed. While sucrose intake is primarily responsible for long-term sleep maintenance, we found that it had no effect on postprandial sleep. Rather, postprandial sleep was positively correlated with ingested volume, protein, and salt—revealing meal property-specific regulation. Silencing of Leucokinin receptor (Lkr) neurons, or Lkr knockdown in these cells, reduced postprandial sleep response specifically to protein ingestion. Paradoxically, silencing a subset of Leucokinin (Lk) neurons increased postprandial sleep, suggesting that Lk has waking outputs normally counterbalanced by Lkr circuitry. This circuitry has also recently been identified as a circadian output module, suggesting that these neurons may serve as an integration point for different types of sleep signaling. These findings reveal the dynamic nature of postprandial sleep and provide a novel system for studying the molecular and neuronal integration of sleep and feeding.