肥胖严重危害着人类的健康，长期以来高脂饮食与运动不足被认为是肥胖发病的主要原因。随着近来儿童肥胖病例的迅速增加，传统肥胖病因学已无法解释此现象。最新动物模型研究发现父源性饮食干预可导致后代(F1)小鼠肝脏代谢相关基因调控区甲基化异常改变且此 F1 小鼠对肥胖易感，推测表观遗传修饰改变可能在环境因素引发的父源性肥胖过程中起着重要作用。本研究将首次从表观遗传继承的视角出发，采用饮食与运动干预的手段，研究6周高脂饮食或/和有氧运动对F0雄性小鼠后代表型和组织基因表达谱的影响，并采用 McMSP 分析研究差异表达基因甲基化修饰改变对代谢相关基因表达的影响，试图揭示父源性高脂饮食影响 F1 小鼠表型及其表观遗传修饰的调控机制。同时，我们将首次探索父系长期规律有氧运动对 F1 小鼠肥胖表型和表观遗传修饰的有益影响，以证实保持健康生活方式不仅对自身有益同时也通过表观遗传继承机制对后代健康产生长远的影响。

Excessive supply of high fat diet(HFD) and lack of exercise caloric consumption has long been recognized as the main factors to obesity, one of the severe chronic diseases threatening human health. Conventional pathophysiology of obesity was challenged by the rapidly increasing number of childhood obesity cases. Current animal model research shows that calory-oversupply patrilineal dietary pattern makes its offspring vulnerable to obesity by inducing an anomalous expression of metablic genes in hepatic tissue, suggesting a crucial role of epigenetic modification in the process of patrilineal obesity in response to environmental factors. From the epigenetic perspective for the first time, dietary and exercise interventions were performed in our research to determine the effects of 6-week HFD with or without aerobic exercise on phenotype and gene expression in the offspring of F0 male mice. To elucidate the underlying regulatory mechanism, McMSP method will be used to analyze the effects of DNA methylation on expression of metabolic specific genes in F1 mice. Also, we will be the first to explore the beneficial impacts of long term regular aerobic exercise on obesity phenotype and epigenetic modification in F1 mice, confirming the concept that the healthy life style is not only benefit to one's own well-being but their offspring through an epigenetic mechanism in long term.