Wang Jiaqi, Shen Chun, Zhao Guangyong, Hanigan Mark D, Li Mengmeng
State Key Laboratory of Animal Nutrition and Feeding, College of Animal Science and Technology, China Agricultural University, Beijing 100193, China.
School of Animal Sciences, Virginia Tech, Blacksburg, VA 24060, USA.
Anim Nutr. 2024 Jul 23;19:117-130. doi: 10.1016/j.aninu.2024.04.028. eCollection 2024 Dec.
This study aimed to develop a compensatory growth model using growing beef cattle by changing dietary protein and to investigate the underlying mechanisms of compensatory protein deposition in muscle tissue. Twelve Charolais bulls were randomly assigned to one of two groups with two periods: 1) a control group (CON) fed a 13% crude protein (CP) diet for 6 weeks; 2) a treatment group (REC) fed a 7% CP diet for 4 weeks (restriction period) and fed a 13% CP diet in the following 2 weeks (re-alimentation period). Growth performance, digestibility, nitrogen balance, targeted metabolomics of amino acids (AA) in plasma, and transcriptional profiling in muscle tissue were analyzed. Protein restriction decreased average daily gain (ADG; < 0.05), while protein re-alimentation increased ADG relative to the CON ( < 0.05). Compared to the CON, REC reduced retained N ( < 0.05), and protein re-alimentation increased retained N and N utilization efficiency ( < 0.05), due to reduced urinary urea, hippuric acid, and creatinine excretions ( < 0.05). Ruminal NH-N in the REC was lower than that in the CON in the protein re-alimentation period ( < 0.05). However, there was no difference in microbial protein and plasma urea nitrogen concentrations. Dietary protein restriction decreased plasma valine and aspartic acid concentrations relative to the CON ( < 0.05), and increased proline and 3-methyl-L-histidine concentrations ( < 0.05). After dietary protein re-alimentation, REC increased plasma citrulline concentrations ( < 0.05). The transcriptional profiling revealed that REC upregulated the AA transporter , and protein re-alimentation downregulated in the muscle cell membrane. Within the muscle cell, upregulated cytosolic arginine sensor for mTORC1 subunit 2 () inhibited protein synthesis by inhibiting the mammalian target of rapamycin complex 1 phosphorylation in the protein restriction period, while DNA-damage-inducible transcript 4 () activated the mTOR signaling pathway and promoted protein synthesis in the protein re-alimentation period. In summary, the targeted metabolomics and transcriptomics analyses demonstrated that protein re-alimentation following restriction can promote protein synthesis and reduce muscle breakdown by regulating AA metabolism and functional transcripts related to AA transporters and the mTOR signaling pathway.
本研究旨在通过改变日粮蛋白质来建立生长肉牛的补偿生长模型，并探究肌肉组织中补偿性蛋白质沉积的潜在机制。将12头夏洛莱公牛随机分为两组，每组两个阶段：1）对照组（CON）饲喂含13%粗蛋白（CP）的日粮6周；2）处理组（REC）饲喂含7%CP的日粮4周（限制期），随后2周饲喂含13%CP的日粮（再饲喂期）。分析了生长性能、消化率、氮平衡、血浆中氨基酸（AA）的靶向代谢组学以及肌肉组织中的转录谱。蛋白质限制降低了平均日增重（ADG；<0.05），而蛋白质再饲喂使ADG相对于CON组增加（<0.05）。与CON组相比，REC组减少了氮保留量（<0.05），蛋白质再饲喂增加了氮保留量和氮利用效率（<0.05），这是由于尿中尿素、马尿酸和肌酐排泄量减少（<0.05）。在蛋白质再饲喂期，REC组瘤胃NH-N低于CON组（<0.05）。然而，微生物蛋白和血浆尿素氮浓度没有差异。与CON组相比，日粮蛋白质限制降低了血浆缬氨酸和天冬氨酸浓度（<0.05），并增加了脯氨酸和3-甲基-L-组氨酸浓度（<0.05）。日粮蛋白质再饲喂后，REC组血浆瓜氨酸浓度增加（<0.05）。转录谱分析显示，REC组上调了肌肉细胞膜上的AA转运体，而蛋白质再饲喂使其下调。在肌肉细胞内，上调的mTORC1亚基2的胞质精氨酸传感器（）在蛋白质限制期通过抑制雷帕霉素靶蛋白复合物1的磷酸化来抑制蛋白质合成，而DNA损伤诱导转录本4（）在蛋白质再饲喂期激活mTOR信号通路并促进蛋白质合成。总之，靶向代谢组学和转录组学分析表明，限制后的蛋白质再饲喂可通过调节AA代谢以及与AA转运体和mTOR信号通路相关的功能转录本来促进蛋白质合成并减少肌肉分解。
