围产期母体饮食对胎儿及新生儿的脂肪分化有着重要影响，我们在人群研究中发现母亲围产期高脂饮食中n-6不饱和脂肪酸的增加与子代肥胖相关，在动物模型中观察到围产期n-6不饱和脂肪酸摄入增加会导致仔鼠脂肪蓄积增加，在体外实验中发现其可上调脂肪细胞分化通路表达，但机制未明。GPR120受体是n-6不饱和脂肪酸的内源性受体，在脂肪细胞分化中扮演着重要作用，我们猜测n-6不饱和脂肪酸通过GPR120受体及其下游通路调控胎儿期及新生儿期的早期脂肪细胞分化。此研究拟使用前脂肪细胞深入研究n-6不饱和脂肪酸通过GPR120的信号通路调控脂肪细胞分化的分子机制，借助GPR120脂肪组织特异性条件敲除小鼠模型在体内实验上加以验证。本课题的研究将有助于理解n-6不饱和脂肪酸在早期脂肪细胞分化中所扮演的角色，为肥胖的早期预防和早期干预提供理论基础。

Maternal diet during gestation and lactation plays an important role in fetal and neonatal adipocyte differentiation. We found in a cohort study that the increase in n-6 unsaturated fatty acids in the maternal high-fat diet during gestation and lactation was associated with obesity in the offspring. We also found that increased intake of n-6 unsaturated fatty acids during gestation and lactation leads to increased fat accumulation in the pups. n-6 unsaturated fatty acids was found to upregulate the expression of adipocyte differentiation pathways in vitro, but the mechanism is unknown. The GPR120 receptor is an endogenous receptor for n-6 unsaturated fatty acids and plays an important role in adipocyte differentiation. We hypothesize that n-6 unsaturated fatty acids regulate early adipocyte differentiation in the fetal and neonatal stages via the GPR120 receptor and its downstream pathway. This study intends to use pre-adipocytes to study the molecular mechanism of n-6 unsaturated fatty acid regulation of adipocyte differentiation through GPR120 signaling pathway, and validate it in vivo by means of GPR120 adipose tissue-specific conditional knockout mouse model. This research will help to understand the role of n-6 unsaturated fatty acids in early adipocyte differentiation, providing a theoretical basis for early prevention and early intervention of obesity.