急性睡眠剥夺重塑与癌症风险相关的代谢和线粒体通路

Sleep deprivation is common and has been linked to elevated cancer risk, yet the immediate mammalian responses that connect acute sleep loss to cancer remain unclear. We asked whether a single 5-hour bout of acute sleep deprivation (ASD) reprograms metabolic and mitochondrial pathways across organs that govern whole-body energetics in a mouse model. Twelve-week C57BL/6 female mice underwent ASD or ad lib sleep; liver, hippocampus, prefrontal cortex, and gastrocnemius were collected immediately and profiled by RT-qPCR for energy sensing (AMPK), glucose transport (GLUT3), mitochondrial dynamics (DRP1/MFN1/OPA1), and hepatic lipid/cholesterol handling (ABCA1/SCARB1/apolipoproteins). ASD triggered rapid, tissue-selective remodeling: AMPK/GLUT3 and mitochondrial-dynamics transcripts rose in brain regions, while hepatic cholesterol transport and apolipoproteins were altered; however skeletal muscle showed minimal change. These coordinated shifts map to cancer-relevant processes-deregulated cellular energetics, mitochondrial quality control/redox, and sterol flux that shapes membrane signaling and tissue inflammation, positioning sleep state as a modifiable, system-wide determinant of cancer susceptibility and progression. Ongoing work will examine whether repeated ASD or sleep restoration tunes these pathways and related tumor-relevant endpoints.