Yang Chao, Zhou Xiaoling, Yang Hong, Gebeyew Kefyalew, Yan Qiongxian, Zhou Chuanshe, He Zhixiong, Tan Zhiliang
CAS Key Laboratory for Agro-Ecological Processes in Subtropical Region, National Engineering Laboratory for Pollution Control and Waste Utilization in Livestock and Poultry Production, South-Central Experimental Station of Animal Nutrition and Feed Science, Institute of Subtropical Agriculture, The Chinese Academy of Sciences, Changsha, Hunan, China.
University of Chinese Academy of Sciences, Beijing, China.
PeerJ. 2021 Jan 29;9:e10593. doi: 10.7717/peerj.10593. eCollection 2021.
Maternal nutrient restriction during pregnancy causes a metabolic disorder that threatens the offspring's health in humans and animals. However, the molecular mechanism of how undernutrition affecting hepatic metabolism of fetal or postnatal offspring is still unclear. We aimed to investigate transcriptomic changes of fetal livers in response to maternal malnutrition in goats during mid-gestation and to explore whether these changes would disappear when the nutrition was recovered to normal level during mid-gestation using goats () as the experimental animals.
Fifty-three pregnant goats were subjected to a control (100% of the maintenance requirements, CON) or a restricted (60% of the maintenance requirements on day 45 to day 100 of gestation and then realimentation, RES) diet. A total of 16 liver samples were collected from fetal goats on day 100 of gestation and goat kids of postnatal day 90 to obtain hepatic transcriptional profiles using RNA-Seq.
Principal component analysis of the hepatic transcriptomes presented a clear separation by growth phase (fetus and kid) rather than treatment. Maternal undernutrition up-regulated 86 genes and down-regulated 76 genes in the fetal liver of the FR group as compared to the FC group. KEGG pathway analysis showed the DEGs mainly enriched in protein digestion and absorption, steroid biosynthesis, carbohydrate digestion and absorption and bile secretion. A total of 118 significant DEGs (fold change > 1.2 and FDR < 0.1) within KR vs. KC comparison was identified with 79 up-regulated genes and down-regulated 39 genes, and these DEGs mainly enriched in the biosynthesis of amino acids, citrate cycle, valine, leucine and isoleucine biosynthesis and carbon metabolism.
Hepatic transcriptome analysis showed that maternal undernutrition promoted protein digestion and absorption in the fetal livers, while which restrained carbohydrate metabolism and citric acid cycle in the livers of kid goats after realimentation. The results indicate that maternal undernutrition during mid-gestation causes hepatic metabolism programming in kid goats on a molecular level.
孕期母体营养限制会引发一种代谢紊乱,对人类和动物后代的健康构成威胁。然而,营养不良如何影响胎儿或产后子代肝脏代谢的分子机制仍不清楚。我们旨在研究妊娠中期山羊母体营养不良时胎儿肝脏的转录组变化,并探讨当妊娠中期营养恢复到正常水平时这些变化是否会消失,以山羊为实验动物。
53只妊娠山羊分别给予对照(维持需要量的100%,CON)或限制(妊娠第45天至第100天给予维持需要量的60%,然后恢复营养,RES)日粮。在妊娠第100天从胎羊和出生后第90天的羔羊中总共收集16个肝脏样本,使用RNA测序获得肝脏转录谱。
肝脏转录组的主成分分析显示,按生长阶段(胎儿和羔羊)而非处理方式有明显区分。与FC组相比,FR组母体营养不良使胎肝中86个基因上调,76个基因下调。KEGG通路分析表明,差异表达基因主要富集于蛋白质消化与吸收、类固醇生物合成、碳水化合物消化与吸收以及胆汁分泌。在KR与KC比较中总共鉴定出118个显著差异表达基因(变化倍数>1.2且FDR<0.1),其中79个基因上调,39个基因下调,这些差异表达基因主要富集于氨基酸生物合成、柠檬酸循环、缬氨酸、亮氨酸和异亮氨酸生物合成以及碳代谢。
肝脏转录组分析表明,母体营养不良促进了胎肝中的蛋白质消化与吸收,而恢复营养后则抑制了羔羊肝脏中的碳水化合物代谢和柠檬酸循环。结果表明,妊娠中期母体营养不良在分子水平上导致了羔羊肝脏代谢编程。