Dietary threonine(Thr) deficiency increases hepatic triglyceride content and reduces sebum and abdominal fat percentages in lean type(LT), but not in fatty type(FT) Pekin ducks. However, the molecular changes regardin...Dietary threonine(Thr) deficiency increases hepatic triglyceride content and reduces sebum and abdominal fat percentages in lean type(LT), but not in fatty type(FT) Pekin ducks. However, the molecular changes regarding the role of Thr in lipid metabolism in LT and FT ducks induced by Thr deficiency remains unknown. This study compared differential expression gene profiles related to lipid metabolism in FT and LT Pekin ducks affected by Thr deficiency. We performed transcriptomic profiling and scanned the gene expression in the liver, sebum, and abdominal fat of Pekin ducks fed either Thr-deficient or Thr-adequate diet for 21 days from 14 to 35 days of age. There were 187, 52, and 50 differentially expressed genes(DEGs) identified in the liver, sebum, and abdominal fat of LT ducks affected by Thr deficiency, of which 12, 9, and 5 genes were involved in lipid metabolism, respectively. Thr deficiency altered the expression of 27, 6, and 3 genes in FT ducks’ liver, sebum, and abdominal fat, respectively. None of the DEGs had a relationship with lipid metabolism in FT ducks. KEGG analysis showed that the DEGs in the LT ducks’ livers were enriched in lipid metabolism pathways(linolenic acid metabolism, glycerophospholipid metabolism, and arachidonic acid metabolism) and amino acid metabolism pathways(biosynthesis of amino acids, phenylalanine metabolism, β-alanine metabolism, and glycine, serine and threonine metabolisms). The DEGs in the sebum and abdominal fat of LT ducks were not enriched in lipid and amino acid metabolic pathways. Additionally, DEGs involved in lipid metabolism were found to be upregulated by Thr deficiency in LT ducks, such as malic enzyme 3(ME3), acyl-Co A synthetase short-chain family member 2(ACSS2) in liver, and lipase member M(LIPM) in sebum. In summary, dietary Thr deficiency regulated the gene expression involved in lipid metabolism in the liver, sebum, and abdominal fat of Pekin ducks in a genotype-dependent manner.展开更多
基金supported by the National Natural Science Foundation of China(31902174)the Natural Science Foundation of Jiangsu Province,China(BK20190902)the Natural Science Foundation of Jiangsu Higher Education Institutions of China(19KJD230003)。
文摘Dietary threonine(Thr) deficiency increases hepatic triglyceride content and reduces sebum and abdominal fat percentages in lean type(LT), but not in fatty type(FT) Pekin ducks. However, the molecular changes regarding the role of Thr in lipid metabolism in LT and FT ducks induced by Thr deficiency remains unknown. This study compared differential expression gene profiles related to lipid metabolism in FT and LT Pekin ducks affected by Thr deficiency. We performed transcriptomic profiling and scanned the gene expression in the liver, sebum, and abdominal fat of Pekin ducks fed either Thr-deficient or Thr-adequate diet for 21 days from 14 to 35 days of age. There were 187, 52, and 50 differentially expressed genes(DEGs) identified in the liver, sebum, and abdominal fat of LT ducks affected by Thr deficiency, of which 12, 9, and 5 genes were involved in lipid metabolism, respectively. Thr deficiency altered the expression of 27, 6, and 3 genes in FT ducks’ liver, sebum, and abdominal fat, respectively. None of the DEGs had a relationship with lipid metabolism in FT ducks. KEGG analysis showed that the DEGs in the LT ducks’ livers were enriched in lipid metabolism pathways(linolenic acid metabolism, glycerophospholipid metabolism, and arachidonic acid metabolism) and amino acid metabolism pathways(biosynthesis of amino acids, phenylalanine metabolism, β-alanine metabolism, and glycine, serine and threonine metabolisms). The DEGs in the sebum and abdominal fat of LT ducks were not enriched in lipid and amino acid metabolic pathways. Additionally, DEGs involved in lipid metabolism were found to be upregulated by Thr deficiency in LT ducks, such as malic enzyme 3(ME3), acyl-Co A synthetase short-chain family member 2(ACSS2) in liver, and lipase member M(LIPM) in sebum. In summary, dietary Thr deficiency regulated the gene expression involved in lipid metabolism in the liver, sebum, and abdominal fat of Pekin ducks in a genotype-dependent manner.
