[Objective] To explore the effect of vitamin A (VA) deficiency during pregnancy on lipid synthesis in the liver tissue of offspring through a rat model of VA deficiency during pregnancy. [Methods] A rat model of VA deficiency during pregnancy was established and divided into three groups: normal VA, VA-deficient, and VA-deficient with supplementation. The blood lipid levels of the offspring were detected; the changes in mRNA expression of lipid synthesis molecules such as ACC, FAS, and SREBP1 in the liver were measured; and the lipid droplet deposition in the liver tissue sections of the offspring after HE staining was observed. [Results] The HDL - C level in the VAD group was significantly lower than that in the VAN group and the VAS group (P0.05). There was a significant difference in TG levels among the three groups (P < 0.05). The expression levels of ACC, FAS, and SREBP1 mRNA in the VAD group increased significantly. There were more lipid droplet depositions in the liver of the VAD group, and some lipid droplet vacuoles in the cytoplasm; while in the VAS group and the VAN group, the liver cells were arranged regularly and no obvious lipid droplet deposition was observed. [Conclusion] VA deficiency during pregnancy can induce the abnormal activation of the liver lipid synthesis pathway in the offspring of rats, resulting in lipid metabolism disorders.
[目的] 通过孕期VA缺乏大鼠模型,探讨孕期VA缺乏对子代肝脏组织中脂质合成的影响。[方法] 建立大鼠孕期VA缺乏模型,分VA正常、VA缺乏、VA缺乏后补充三组,检测子代血脂水平;肝脏中ACC、FAS、SREBP1等脂质合成分子的mRNA表达变化;观察子代肝脏组织切片HE染色后脂滴沉积情况。[结果] VAD组的HDL-C水平显著低于VAN组和VAS组(P0.05)。TG水平在三组间有显著性差异(P<0.05)。VAD组ACC、FAS、SREBP1 mRNA表达水平显著增加。VAD组肝脏出现较多的脂滴沉积,胞浆中有部分脂滴空泡;而VAS组和VAN组肝细胞排列规则,未见明显脂滴沉积。[结论] 孕期VA缺乏可诱发大鼠子代肝脏脂质合成通路的异常活化,造成质脂代谢紊乱。