Park Scarlet J, Murphy Keith R, Ja William W
Department of Neuroscience, The Herbert Wertheim UF Scripps Institute for Biomedical Innovation & Technology, Jupiter, FL 33458, USA.
Skaggs Graduate School of Chemical and Biological Sciences, Jupiter, FL 33458, USA.
bioRxiv. 2024 Jun 27:2024.05.30.596666. doi: 10.1101/2024.05.30.596666.
Sleep and feeding are vital homeostatic behaviors, and disruptions in either can result in substantial metabolic consequences. Distinct neuronal manipulations in can dissociate sleep loss from subsequent homeostatic rebound, offering an optimal platform to examine the precise interplay between these fundamental behaviors. Here, we investigate concomitant changes in sleep and food intake in individual animals, as well as respiratory metabolic expenditure, that accompany behavioral and genetic manipulations that induce sleep loss in . We find that sleep disruptions resulting in energy deficit through increased metabolic expenditure and manifested as increased food intake were consistently followed by rebound sleep. In contrast, "soft" sleep loss, which does not induce rebound sleep, is not accompanied by increased metabolism and food intake. Our results demonstrate that homeostatic sleep rebound is linked to energy deficit accrued during sleep loss. Collectively, these findings support the notion that sleep functions to conserve energy and highlight the need to examine the effects of metabolic therapeutics on sleep.
睡眠和进食是至关重要的稳态行为，其中任何一项受到干扰都可能导致重大的代谢后果。对[具体内容未提及]进行不同的神经元操作，可以将睡眠缺失与随后的稳态反弹区分开来，为研究这些基本行为之间的精确相互作用提供了一个理想的平台。在这里，我们研究了个体动物在行为和基因操作诱导[具体内容未提及]睡眠缺失时，睡眠和食物摄入量的伴随变化，以及呼吸代谢消耗。我们发现，通过增加代谢消耗导致能量不足并表现为食物摄入量增加的睡眠中断，之后总是伴随着睡眠反弹。相比之下，不引起睡眠反弹的“轻度”睡眠缺失，并未伴随代谢和食物摄入量的增加。我们的结果表明，稳态睡眠反弹与睡眠缺失期间积累的能量不足有关。总的来说，这些发现支持了睡眠具有保存能量功能的观点，并强调了研究代谢疗法对睡眠影响的必要性。
