Multi-omics profiling highlights lipid metabolism alterations in pigs fed low-dose antibiotics
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RESEARCH ARTICLE
Open Access
Multi-omics profiling highlights lipid metabolism alterations in pigs fed low-dose antibiotics Yue Hu1†, Yihe Zhang1†, Cong Liu1, Rui Qin1, Desheng Gong1, Ru Wang2, Du Zhang1, Lianqiang Che2, Daiwen Chen2, Guizhong Xin3, Fei Gao1,4 and Qi Hu1*
Abstract Background: In order to study the relations of hepatocellular functions, weight gain and metabolic imbalance caused by low-dose antibiotics (LDA) via epigenetic regulation of gene transcription, 32 weaned piglets were employed as animal models and randomly allocated into two groups with diets supplemented with 0 or LDA (chlorotetracycline and virginiamycin). Results: During the 4 weeks of the experiment, LDA showed a clear growth-promoting effect, which was exemplified by the significantly elevated body weight and average daily gain. Promoter methylome profiling using liquid hybridization capture-based bisulfite sequencing (LHC-BS) indicated that most of the 745 differential methylation regions (DMRs) were hypermethylated in the LDA group. Several DMRs were significantly enriched in genes related with fatty acids metabolic pathways, such as FABP1 and PCK1. In addition, 71 differentially expressed genes (DEGs) were obtained by strand-specific transcriptome analysis of liver tissues, including ALOX15, CXCL10 and NNMT, which are three key DEGs that function in lipid metabolism and immunity and which had highly elevated expression in the LDA group. In accordance with these molecular changes, the lipidome analyses of serum by LC-MS identified 38 significantly differential lipids, most of which were downregulated in the LDA group. Conclusions: Our results indicate that LDA could induce epigenetic and transcriptional changes of key genes and lead to enhanced efficiency of lipid metabolism in the liver. Keywords: Weaned piglets, Low-dose antibiotics, Serum lipidome, Liver methylome, Liver transcriptome
Background Accumulating evidence has shown a strong crosstalk between gut microbiota and host metabolism [1–4], which can provide clues as to how subtherapeutic antibiotics can promote animal growth [5] and they are associated with risks of obesity in prepubertal children [6–8]. In particular, studies have shown that antibiotic exposure can further affect liver * Correspondence: [email protected] † Yue Hu and Yihe Zhang contributed equally to this work. 1 Genome Analysis Laboratory of the Ministry of Agriculture, Agricultural Genomics Institute at Shenzhen, Chinese Academy of Agricultural Sciences, Shenzhen 518120, China Full list of author information is available at the end of the article
functions due to the gut-liver axis [9]. However, genomescale molecular changes of the liver under antibiotic exposure have not been comprehensively studied. In recent years, crosstalk between the gut microbiota and host epigenome has also been proposed. Many studies have demonstrated that the products of bacterial fermentation, short chain fatty acids (SCFAs), can affect histone modifications by inhibiting mammalian histone deacetylases (HDAC) [10, 11]. As a ma
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