Project to be confirmed after rotation year

流行病学研究提供了强有力的证据，证明肥胖母亲生下的婴儿成年后本身就容易肥胖和代谢健康不良，这种现象可以在小鼠模型中复制。这表明肥胖母亲的成年后代的组织“记住”了生命早期的不利条件。然而，人们对将早期生活事件与成年代谢状态联系起来的分子机制知之甚少。我们将检验这一假设，即在发育过程中，后代组织和干细胞获得代谢衍生的表观遗传标记，这些标记繁殖到成年器官并改变肥胖风险。

Epidemiological studies provide strong evidence that obese mothers give birth tobabies who are themselves predisposed to obesity and poor metabolic health asadults, and this phenomenon can be replicated in mouse models. This suggests thatthe tissues in the adult offspring of obese mothers 'remember' the adverse conditionsduring early life. However, the molecular mechanisms that link early life events toadult metabolic state are poorly understood. We will test the hypothesis that duringdevelopment offspring tissues and stem cells acquire metabolite-derived epigeneticmarks that are propagated to adult organs and modify obesity risk.