睡眠剥夺对代谢功能的影响是国外睡眠医学研究关注的一个重要方向，但国内在此领域的研究较少。申请人在开展睡眠剥夺应激条件下肝脏代谢功能失衡效应的前期工作中发现胆汁酸稳态受到显著影响，具体表现为：血液胆汁酸水平显著下降，肝脏胆汁酸合成经典途径限速酶CYP7A1的表达受到显著抑制。microRNA是近些年脂代谢研究的全新视角。申请人在筛选肝脏差异因子的过程中发现，睡眠剥夺应激条件下肝脏miR-122表达水平显著下降，并利用miR-122 mimics转染HepG2细胞（低表达miR-122）证实过表达miR-122后CYP7A1表达水平显著上调。以上结果提示，miR-122可能通过间接调控CYP7A1表达在胆汁酸合成代谢中发挥作用。本项目拟对miR-122在睡眠剥夺诱发肝脏胆汁酸合成代谢异常中的作用机制及生物学意义进行分析，期望阐明miR-122调控胆汁酸合成代谢的作用机制。

The harmful effects of sleep deprivation on metabolic function is an important content in the research field of sleep medicine abroad, but the domestic research in this field is rather less. In the previous study on metabolic imbalance induced by sleep deprivation, we found that the bile acids homeostasis was significantly affected, which was characterized with significant decrease of bile acid in the serum and the inhibition on the expression of bile acid synthesis rate limiting enzyme CYP7A1 of the classical pathway. MicroRNA provides a new perspective in the study of lipid metabolism in recent years. While analyzing the difference factor in the liver under the stress conditions of sleep deprivation, we found that miR-122 expression in liver significantly decreased. And the CYP7A1 expression in HepG2 cells transfected with miR-122 mimics was significantly increased. The above results suggested that miR-122 was involved in the abnormal bile acid metabolism induced by sleep deprivation. The current project aims to explore the mechanisms and biological significance of miR-122 in regulating the abnormal metabolism of bile acid synthesis induced by sleep deprivation.