Gunawan Shirley Priscilla, Huang Shih-Yi, Hsu Jhih-Wei, Lin Chia-Yuan, Nguyen Nam Nhat, Tung Te-Hsuan, Liang Shu-Ling, Lee Gilbert Aaron, Su Chien-Tien, Chen Yang Ching
Graduate Institute of Metabolism and Obesity Sciences, Taipei Medical University, Taipei, Taiwan.
School of Nutrition and Health Sciences, Taipei Medical University, Taipei, Taiwan.
PeerJ. 2025 Jul 9;13:e19668. doi: 10.7717/peerj.19668. eCollection 2025.
Chronic sleep deprivation (CSD) in adolescents has become a trend with adverse health outcomes. Previous studies have demonstrated that sleep deprivation causes inflammation, alters puberty onset, and changes the gut microbiome composition; however, the relationship between these is still unknown. Therefore, we hypothesized that CSD delays the onset of puberty elevating proinflammatory cytokines and alter ation of gut microbiome composition. Using the modified multiple platform method, we conducted a 4-week CSD experiment in juvenile rats and assessed pubertal markers, antioxidant activity, cytokine levels, and gut microbiome profiles. CSD significantly reduces body weight, delays onset of puberty, and elevated antioxidant enzyme activities in both sexes. In the sleep-deprivation female (SDF) rats, plasma levels of lipopolysaccharide-binding protein (LBP), interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) were significantly elevated; mRNA levels of - and were also significantly elevated in the colon and reproductive organs, respectively. In the sleep-deprivation male (SDM) rats, only plasma levels of IL-6 were elevated considerably; in addition, mRNA levels of and - were also significantly elevated in the colon and reproductive organs, respectively. Gut microbiome analysis revealed that the predominant bacteria at the genus level were , , and in the SDF rats; , , , and in the SDM rats. CSD rats with abundant genera were positively correlated with antioxidant enzyme activities and mRNA levels of proinflammatory cytokines. Overall, CSD is associated with delayed puberty onset, possibly an increase in the expression levels of proinflammatory cytokines and altering the gut microbiome composition, indicating proinflammatory cytokines and gut microbiome play an important role in pubertal timing change. These findings may guide the future studies to intervene sleep deprivation-related delays in the onset of puberty.
青少年慢性睡眠剥夺（CSD）已成为一种趋势，并会带来不良健康后果。先前的研究表明，睡眠剥夺会引发炎症、改变青春期开始时间，并改变肠道微生物群组成；然而，这些因素之间的关系仍不清楚。因此，我们推测CSD会通过升高促炎细胞因子和改变肠道微生物群组成来延迟青春期开始。我们使用改良的多平台方法，对幼年大鼠进行了为期4周的CSD实验，并评估了青春期标志物、抗氧化活性、细胞因子水平和肠道微生物群谱。CSD显著降低了两性的体重，延迟了青春期开始，并提高了抗氧化酶活性。在睡眠剥夺雌性（SDF）大鼠中，血浆脂多糖结合蛋白（LBP）、白细胞介素-1β（IL-1β）、白细胞介素-6（IL-6）和肿瘤坏死因子-α（TNF-α）水平显著升高；结肠和生殖器官中-和的mRNA水平也分别显著升高。在睡眠剥夺雄性（SDM）大鼠中，只有IL-6的血浆水平显著升高；此外，结肠和生殖器官中-和-的mRNA水平也分别显著升高。肠道微生物群分析显示，SDF大鼠中属水平上的主要细菌是、和；SDM大鼠中是、、和。具有丰富属的CSD大鼠与抗氧化酶活性和促炎细胞因子的mRNA水平呈正相关。总体而言，CSD与青春期开始延迟有关，可能是促炎细胞因子表达水平增加和肠道微生物群组成改变所致，表明促炎细胞因子和肠道微生物群在青春期时间变化中起重要作用。这些发现可能会指导未来关于干预与睡眠剥夺相关的青春期开始延迟的研究。
