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; P < 0.05), while protein re-alimentation increased ADG relative to the CON (P < 0.05). Compared to the CON, REC reduced retained N (P < 0.05), and protein re-alimentation increased retained N and N utilization efficiency (P < 0.05), due to reduced urinary urea, hippuric acid, and creatinine excretions (P < 0.05). Ruminal NH₃-N in the REC was lower than that in the CON in the protein re-alimentation period (P < 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 (P < 0.05), and increased proline and 3-methyl-L-histidine concentrations (P < 0.05). After dietary protein re-alimentation, REC increased plasma citrulline concentrations (P < 0.05). The transcriptional profiling revealed that REC upregulated the AA transporter SLC3A1, and protein re-alimentation downregulated SLC7A8 in the muscle cell membrane. Within the muscle cell, upregulated cytosolic arginine sensor for mTORC1 subunit 2 (CASTOR2) inhibited protein synthesis by inhibiting the mammalian target of rapamycin complex 1 phosphorylation in the protein restriction period, while DNA-damage-inducible transcript 4 (DDIT4) 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.

Keywords: Amino acid; Beef cattle; Compensatory growth; Metabolism; Protein.

© 2024 The Authors.

本研究旨在通过改变日粮蛋白质水平来开发一种补偿性生长模型，并探讨肌肉组织中补偿性蛋白沉积的潜在机制。选取12头夏洛莱公牛，随机分配到两个组别和两个时期：1）对照组（CON），喂养粗蛋白含量为13%的日粮6周；2）处理组（REC），先喂养粗蛋白含量为7%的日粮4周（限制期），随后喂养13%的粗蛋白日粮2周（再饲期）。研究分析了生长性能、消化率、氮平衡、血浆中氨基酸（AA）的目标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每天增重（ADG，P < 0.05），而蛋白质再饲增加了与对照组相比的ADG (P < 0.05)。与对照组相比，处理组减少了保留氮量(P < 0.05)，并且在蛋白再饲期增加了保留氮和氮利用率（P < 0.05），这是由于尿素、马尿酸以及肌酐排泄减少所致(P < 0.05)。蛋白质再饲期内REC中的瘤胃NH₃-N含量低于对照组(P < 0.05)，但微生物蛋白和血浆尿素氮浓度没有差异。日粮中蛋白质限制降低了相对于对照组的缬氨酸和天冬氨酸在血浆中的浓度（P < 0.05），同时增加了脯氨酸及3-甲基-L-组氨酸的含量(P < 0.05)。在饮食蛋白再饲期后，REC使血浆瓜氨酸浓度增加(P < 0.05)。转录谱分析显示，处理组上调了AA转运体SLC3A1，而在蛋白质再饲期下调了肌细胞膜中的SLC7A8。在肌细胞内，在限制期内，上调的胞质精氨酸mTORC1亚基2（CASTOR2）通过抑制哺乳动物雷帕霉素靶点复合物1磷酸化来抑制蛋白合成，而在蛋白质再饲期间DNA损伤诱导转录4（DDIT4）激活了mTOR信号通路并促进蛋白质合成。总之，目标代谢组学和转录组学分析表明，在限制后进行的蛋白质再饲可以通过调节氨基酸代谢及相关转运体的功能转录本以及mTOR信号途径来促进蛋白合成并减少肌肉分解。

关键词：氨基酸；肉牛；补偿性生长；代谢；蛋白质。