The objective of this study was to reveal the effect of rumen degradable starch (RDS) on bile acid metabolism and liver transcription in dairy goats using metabolomics and transcriptomics. Eighteen Guanzhong dairy goats of a similar weight and production level (body weight = 45.8 ± 1.54 kg, milk yield = 1.75 ± 0.08 kg, and second parity) were randomly assigned to 3 treatment groups where they were fed a low RDS (LRDS, RDS = 20.52% DM) diet, medium RDS (MRDS, RDS = 22.15% DM) diet, or high RDS (HRDS, RDS = 24.88% DM) diet, respectively. The goats were fed with the experimental diets for 5 weeks. On the last day of the experiment, all goats were anesthetized, and peripheral blood and liver tissue samples were collected. The peripheral blood samples were used in metabolomic analysis and white blood cell (WBC) count, whereas the liver tissue samples were used in transcriptomic analysis. Based on the metabolomics results, the relative abundances of primary bile acids in the peripheral blood were significantly reduced in the group that was fed the HRDS diet (P < 0.05). The WBC count was significantly increased in the HRDS group compared with that in the LRDS and MRDS groups (P < 0.01), indicating that there was inflammation in the HRDS group. Transcriptomic analysis showed that 4 genes related to bile acid secretion (genes: MDR1, RXRα, AE2, SULT2A1) were significantly downregulated in the HRDS group. In addition, genes related to the immune response were upregulated in the HRDS group, suggesting the HRDS diet induced a hepatic inflammatory response mediated by lipopolysaccharides (LPS) (gene: LBP), activated the Toll-like receptor 4 binding (genes: S100A8, S100A9) and the NF-kappa B signaling pathway (genes: LOC106503980, LOC108638497, CD40, LOC102180880, LOC102170970, LOC102175177, LBP, LOC102168903, LOC102185461, LY96 and CXCL8), triggered inflammation and complement responses (genes: C1QB, C1QC, and CFD). The HRDS diet induced a hepatic inflammatory response may be mediated by activating the Toll-like receptor 4 binding and NF-kappa B signaling pathway after free LPS entered the liver. The changes of bile acids profile in blood and the down-regulation of 4 key genes (MDR1, RXRα, AE2, SULT2A1) involved in bile secretion in liver are probably related to liver inflammation.

本研究的目的是利用代谢组学和转录组学揭示瘤胃可降解淀粉（RDS）对奶山羊胆汁酸代谢和肝脏转录的影响。将 18 只体重和生产水平相似的关中奶山羊（体重 = 45.8 ± 1.54 kg，产奶量 = 1.75 ± 0.08 kg，二胎）随机分为 3 个处理组，饲喂低 RDS（LRDS、RDS）。 = 20.52% DM）饮食、中等 RDS（MRDS、RDS = 22.15% DM）饮食或高 RDS（HRDS、RDS = 24.88% DM）饮食。用实验饲料喂养山羊 5 周。实验最后一天，麻醉所有山羊，采集外周血和肝组织样本。外周血样本用于代谢组学分析和白细胞（WBC）计数，而肝组织样本用于转录组学分析。根据代谢组学结果，喂食 HRDS 饮食的组外周血中初级胆汁酸的相对丰度显着降低（P  < 0.05）。HRDS 组 WBC 计数较 LRDS 和 MRDS 组显着升高（P  < 0.01），表明 HRDS 组存在炎症。转录组分析显示， HRDS组中与胆汁酸分泌相关的4个基因（基因：MDR1、RXRα、AE2、SULT2A1 ）显着下调。此外，与免疫反应相关的基因在HRDS组中上调，表明HRDS饮食诱导了脂多糖（LPS）介导的肝脏炎症反应（基因：LBP），激活了Toll样受体4结合（基因：S100A8，S100A9）和 NF-κ B 信号通路（基因：LOC106503980、LOC108638497、CD40、LOC102180880、LOC102170970、LOC102175177、LBP、LOC102168903、LOC102185461、LY96 和CXCL 8 )，引发炎症和补体反应（基因：C1QB、C1QC和CFD）。HRDS饮食诱导的肝脏炎症反应可能是通过游离LPS进入肝脏后激活Toll样受体4结合和NF-κB信号通路介导的。血液中胆汁酸谱的变化以及肝脏中参与胆汁分泌的4个关键基因（ MDR1、RXRα、AE2、SULT2A1 ）的下调可能与肝脏炎症有关。