细胞有氧代谢和无氧代谢稳态有精确的调控机制。氧代谢的失衡会导致肌肉耐力和协调性的变化，心力储备、肝糖元储备和呼吸能力异常等各种慢性疾病。生物钟与机体的基础代谢和氧代谢有紧密联系，但是生物钟如何调控氧代谢的分子机制依然是一个未知的领域。本项目将利用基因敲除和转基因小鼠模型系统研究生物钟基因Per2节律与细胞的氧代谢节律的同步性，确定Per2基因在机体整体水平上对氧代谢的调控；通过对野生型小鼠、Per2基因缺失小鼠和Per2过表达小鼠在葡萄糖刺激下的代谢组学分析，进一步验证生物钟基因Per2对有氧代谢和无氧代谢的影响，阐明Per2通过调控PDK等相关基因的表达来影响机体氧代谢的分子机制。通过研究在衰老的小鼠中补偿Per2基因表达对小鼠氧代谢水平的恢复，进一步确定Per2基因对氧代谢调控的证据。其研究结果将丰富我们对衰老与生物钟关系的认识，从而在生物钟系统调控机体代谢的分子机制方面有新的突破。

The homeostasis of aerobic metabolism and anaerobic metabolism has precise mechanism of regulation. The unbalanced oxygen metabolism results in a significant change of muscular endurance and coordination, as well as in the abnormality of cardiac reserve, liver glycogen reserves and breathe ability, which can induce many chronic diseases. Circadian clock is closely related to basal metabolism and oxygen metabolism. However, the mechanism of circadian clock gene Per2 regulates oxygen metabolism remains unclear. The project will use the knockout mice and transgenic mice to study the synchronization of circadian clock gene Per2 rhythm and oxygen metabolism rhythm, the effect of the Per2 gene on the body oxygen metabolism on the overall level can be confirmed. Moreover, we will use wild-type mice，Per2-null mice and Per2 over-expression mice to investigate metabonomics assay with glucose stimulation. This can validate the metabolism of Per2 gene regulates aerobic and anaerobic metabolism. These will illuminate the mechanisms of Per2 gene regulate aerobic and anaerobic metabolism is through regulating the expression of PDK-associated gene. Additionally, we use the aging mice to compensate Per2 gene expression to investigate the reversal of oxygen metabolism, which can ascertain the regulation of Per2 gene on oxygen metabolism. These results will enrich our understanding of the relationship between aging and circadian clock, provide new insights on the mechanism of circadian clock regulating metabolic rate.