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转录组分析揭示了北京鸭在日粮苏氨酸缺乏期间肝脏甘油三酯代谢调控基因的差异表达。

Transcriptome Analysis Reveals Differential Expression of Genes Regulating Hepatic Triglyceride Metabolism in Pekin Ducks During Dietary Threonine Deficiency.

作者信息

Jiang Yong, Xie Ming, Fan Wenlei, Xue Jiajia, Zhou Zhengkui, Tang Jing, Chen Guohong, Hou Shuisheng

机构信息

Key Laboratory of Animal (Poultry) Genetics Breeding and Reproduction, Ministry of Agriculture and Rural Affairs; Institute of Animal Sciences, Chinese Academy of Agricultural Sciences, Beijing, China.

College of Animal Science and Technology, Yangzhou University, Yangzhou, China.

出版信息

Front Genet. 2019 Aug 2;10:710. doi: 10.3389/fgene.2019.00710. eCollection 2019.

DOI:10.3389/fgene.2019.00710
PMID:31428138
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6688585/
Abstract

Dietary threonine (Thr) deficiency increases hepatic triglyceride accumulation in Pekin ducks, which results in fatty liver disease and impairs hepatic function. However, the underlying molecular mechanisms altered by dietary Thr deficiency are still unknown. To identify the underlying molecular changes, 180 one-day-old ducklings were divided into three groups, including Thr deficiency group (Thr-D), Thr sufficiency group (Thr-S), and pair-fed group (Pair-F) that was fed with a Thr-sufficient diet but with reduced daily feed intake. The results showed that feed intake was similar between Thr-D and Pair-F groups, but weight gain rate and final body weight in the Thr-D group were lower than those in the Pair-F group. Feed intake, weight gain, and body weight in Thr-D and Pair-F groups were lower than those in the Thr-S group. The Thr-D diet reduced abdominal fat percentage but increased hepatic triglyceride content when compared with that of the Thr-S and Pair-F groups. The Pair-F reduced hepatic levels of C15:0, C17:0, C18:0, C20:0, C20:4n6, and C22:0 and also reduced total fatty acid, saturated fatty acid, and unsaturated fatty acid content when compared with those of the Thr-D and Thr-S groups. The Thr-D diet increased hepatic content of C6:0, C17:1, C18:3n6, C20:0, C20:1n9, and C22:2, as well as reduced the content of C18:2n6t and C23:0 when compared with those of the Thr-S group. Transcriptome analysis in the liver indicated that the Thr-D diet upregulated genes related to fatty acid and triglyceride synthesis and downregulated genes related to fatty acid oxidation and triglyceride transport. Gene ontology analysis showed that more genes related to lipid metabolism processes and molecular function were differentially expressed in the Thr-D group relative to Thr-S and Pair-F groups than in the Pair-F group relative to the Thr-S group. KEGG pathway analysis showed that differentially expressed genes were enriched in signal transduction, immune, hormone, lipid, and amino acid metabolism pathways. Our findings indicated that the Thr-D diet increased hepatic triglyceride and fatty acid accumulation increasing fatty acid and triglyceride synthesis and reducing fatty acid oxidation and triglyceride transport. These findings provide novel insights into our understanding of the molecular mechanisms underlying fat accumulation in the liver caused by dietary threonine deficiency.

摘要

日粮苏氨酸(Thr)缺乏会增加北京鸭肝脏甘油三酯的积累,导致脂肪肝疾病并损害肝功能。然而,日粮Thr缺乏所改变的潜在分子机制仍不清楚。为了确定潜在的分子变化,将180只1日龄雏鸭分为三组,包括Thr缺乏组(Thr-D)、Thr充足组(Thr-S)和配对饲喂组(Pair-F),配对饲喂组饲喂Thr充足的日粮,但每日采食量减少。结果表明,Thr-D组和Pair-F组的采食量相似,但Thr-D组的体重增加率和最终体重低于Pair-F组。Thr-D组和Pair-F组的采食量、体重增加和体重均低于Thr-S组。与Thr-S组和Pair-F组相比,Thr-D日粮降低了腹部脂肪百分比,但增加了肝脏甘油三酯含量。与Thr-D组和Thr-S组相比,Pair-F组降低了肝脏中C15:0、C17:0、C18:0、C20:0、C20:4n6和C22:0的水平,也降低了总脂肪酸、饱和脂肪酸和不饱和脂肪酸含量。与Thr-S组相比,Thr-D日粮增加了肝脏中C6:0、C17:1、C18:3n6、C20:0、C20:1n9和C22:2的含量,同时降低了C18:2n6t和C23:0的含量。肝脏转录组分析表明,Thr-D日粮上调了与脂肪酸和甘油三酯合成相关的基因,下调了与脂肪酸氧化和甘油三酯转运相关的基因。基因本体分析表明,相对于Thr-S组和Pair-F组,Thr-D组中更多与脂质代谢过程和分子功能相关的基因差异表达,而相对于Thr-S组,Pair-F组中差异表达的基因较少。KEGG通路分析表明,差异表达基因富集于信号转导、免疫、激素、脂质和氨基酸代谢通路。我们的研究结果表明,Thr-D日粮增加了肝脏甘油三酯和脂肪酸的积累,增加了脂肪酸和甘油三酯的合成,减少了脂肪酸氧化和甘油三酯转运。这些发现为我们理解日粮苏氨酸缺乏导致肝脏脂肪积累的分子机制提供了新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/824e/6688585/7555d43a5b71/fgene-10-00710-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/824e/6688585/baf7dfa43aa6/fgene-10-00710-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/824e/6688585/eea690936203/fgene-10-00710-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/824e/6688585/57517a31e901/fgene-10-00710-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/824e/6688585/89ee28b83609/fgene-10-00710-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/824e/6688585/7555d43a5b71/fgene-10-00710-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/824e/6688585/baf7dfa43aa6/fgene-10-00710-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/824e/6688585/eea690936203/fgene-10-00710-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/824e/6688585/57517a31e901/fgene-10-00710-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/824e/6688585/89ee28b83609/fgene-10-00710-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/824e/6688585/7555d43a5b71/fgene-10-00710-g005.jpg

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