Sleep is vital for survival. Yet under environmentally challenging conditions, such as starvation, animals suppress their need for sleep. Interestingly, starvation-induced sleep loss does not evoke a subsequent sleep rebound. Little is known about how starvation-induced sleep deprivation differs from other types of sleep loss, or why some sleep functions become dispensable during starvation. Here, we demonstrate that down-regulation of the secreted cytokine unpaired 2 (upd2) in Drosophila flies may mimic a starved-like state. We used a genetic knockdown strategy to investigate the consequences of upd2 on visual attention and sleep in otherwise well-fed flies, thereby sidestepping the negative side effects of undernourishment. We find that knockdown of upd2 in the fat body (FB) is sufficient to suppress sleep and promote feeding-related behaviors while also improving selective visual attention. Furthermore, we show that this peripheral signal is integrated in the fly brain via insulin-expressing cells. Together, these findings identify a role for peripheral tissue-to-brain interactions in the simultaneous regulation of sleep quality and attention, to potentially promote adaptive behaviors necessary for survival in hungry animals.

睡眠对于生存至关重要。然而，在饥饿等环境挑战条件下，动物会抑制睡眠需求。有趣的是，饥饿引起的睡眠不足并不会引起随后的睡眠反弹。人们对饥饿引起的睡眠剥夺与其他类型的睡眠不足有何不同，或者为什么某些睡眠功能在饥饿期间变得可有可无，知之甚少。在这里，我们证明果蝇中分泌的细胞因子未配对 2 ( upd2 ) 的下调可能模拟饥饿状态。我们使用基因敲低策略来研究upd2对营养良好的果蝇的视觉注意力和睡眠的影响，从而避免营养不良的负面影响。我们发现，敲低脂肪体（FB）中的upd2足以抑制睡眠并促进进食相关行为，同时还能提高选择性视觉注意力。此外，我们发现这种外周信号通过胰岛素表达细胞整合到果蝇大脑中。总之，这些发现确定了外周组织与大脑的相互作用在睡眠质量和注意力的同时调节中的作用，可能促进饥饿动物生存所需的适应性行为。