Periparturient cows release fatty acid reserves from adipose tissue (AT) through lipolysis in response to the negative energy balance induced by physiological changes related to parturition and the onset of lactation. However, lipolysis causes inflammation and structural remodeling in AT that in excess predisposes cows to disease. The objective of this study was to determine the effects of the periparturient period on the transcriptomic profile of AT using NGS RNAseq. Subcutaneous AT samples were collected from Holstein cows (n = 12) at 11 ± 3.6 d before calving date (PreP) and at 6 ± 1d (PP1) and 13 ± 1.4d (PP2) after parturition. Differential expression analyses showed 1946 and 1524 DEG at PP1 and PP2, respectively, compared to PreP. Functional Enrichment Analysis revealed functions grouped in categories such as lipid metabolism, molecular transport, energy production, inflammation, and free radical scavenging to be affected by parturition and the onset of lactation (FDR < 0.05). Inflammation related genes such as TLR4 and IL6 were categorized as upstream lipolysis triggers. In contrast, FASN, ELOVL6, ACLS1, and THRSP were identified as upstream inhibitors of lipid synthesis. Complement (C3), CXCL2, and HMOX1 were defined as links between inflammatory pathways and those involved in the generation of reactive oxygen species. Results offer a comprehensive characterization of gene expression dynamics in periparturient AT, identify upstream regulators of AT function, and demonstrate complex interactions between lipid mobilization, inflammation, extracellular matrix remodeling, and redox signaling in the adipose organ.

中文翻译：

---

围产期奶牛（Bos taurus）的脂肪组织炎症，重塑和脂质代谢的转录组分析

围产期母牛通过脂解作用从脂肪组织（AT）释放脂肪酸储备，以响应与分娩和泌乳开始有关的生理变化引起的负能量平衡。但是，脂肪分解会引起AT的炎症和结构重塑，过多会使母牛患病。这项研究的目的是使用NGS RNAseq确定围产期对AT转录组谱的影响。在分娩日期前11±3.6 d（PreP）和分娩后6±1d（PP1）和13±1.4d（PP2）从荷斯坦奶牛（n = 12）收集皮下AT样品。与PreP相比，差异表达分析显示PP1和PP2分别为1946和1524 DEG。功能富集分析揭示了功能分类，例如脂质代谢，分子运输，能量产生，炎症和自由基清除受到分娩和泌乳期的影响（FDR <0.05）。炎症相关基因，例如TLR4和IL6被归类为上游脂解触发。相反，FASN，ELOVL6，ACLS1和THRSP被确定为脂质合成的上游抑制剂。补体（C3），CXCL2和HMOX1被定义为炎症途径与参与活性氧物种产生的途径之间的联系。结果提供了围产期AT中基因表达动力学的全面表征，确定了AT功能的上游调节剂，并证明了脂肪器官中脂质动员，炎症，细胞外基质重塑和氧化还原信号之间的复杂相互作用。和自由基清除受到分娩和泌乳期的影响（FDR <0.05）。炎症相关基因，例如TLR4和IL6被归类为上游脂解触发。相反，FASN，ELOVL6，ACLS1和THRSP被确定为脂质合成的上游抑制剂。补体（C3），CXCL2和HMOX1被定义为炎症途径与参与活性氧物种产生的途径之间的联系。结果提供了围产期AT中基因表达动力学的全面表征，确定了AT功能的上游调节剂，并证明了脂肪器官中脂质动员，炎症，细胞外基质重塑和氧化还原信号之间的复杂相互作用。和自由基清除受到分娩和泌乳期的影响（FDR <0.05）。炎症相关基因，例如TLR4和IL6被归类为上游脂解触发。相反，FASN，ELOVL6，ACLS1和THRSP被确定为脂质合成的上游抑制剂。补体（C3），CXCL2和HMOX1被定义为炎症途径与参与活性氧物种产生的途径之间的联系。结果提供了围产期AT中基因表达动力学的全面表征，确定了AT功能的上游调节剂，并证明了脂肪器官中脂质动员，炎症，细胞外基质重塑和氧化还原信号之间的复杂相互作用。炎症相关基因，例如TLR4和IL6被归类为上游脂解触发。相反，FASN，ELOVL6，ACLS1和THRSP被确定为脂质合成的上游抑制剂。补体（C3），CXCL2和HMOX1被定义为炎症途径与参与活性氧物种产生的途径之间的联系。结果提供了围产期AT中基因表达动力学的全面表征，确定了AT功能的上游调节剂，并证明了脂肪器官中脂质动员，炎症，细胞外基质重塑和氧化还原信号之间的复杂相互作用。炎症相关基因，例如TLR4和IL6被归类为上游脂解触发。相反，FASN，ELOVL6，ACLS1和THRSP被确定为脂质合成的上游抑制剂。补体（C3），CXCL2和HMOX1被定义为炎症途径与参与活性氧物种产生的途径之间的联系。结果提供了围产期AT中基因表达动力学的全面表征，确定了AT功能的上游调节剂，并证明了脂肪器官中脂质动员，炎症，细胞外基质重塑和氧化还原信号之间的复杂相互作用。HMOX1和HMOX1被定义为炎症途径与活性氧产生途径之间的联系。结果提供了围产期AT中基因表达动力学的全面表征，确定了AT功能的上游调节剂，并证明了脂肪器官中脂质动员，炎症，细胞外基质重塑和氧化还原信号之间的复杂相互作用。HMOX1和HMOX1被定义为炎症途径与活性氧产生途径之间的联系。结果提供了围产期AT中基因表达动力学的全面表征，确定了AT功能的上游调节剂，并证明了脂肪器官中脂质动员，炎症，细胞外基质重塑和氧化还原信号之间的复杂相互作用。