Creatine stores high-energy phosphate bonds in muscle and is synthesized in the liver through methylation of guanidinoacetic acid (GAA). Supplementation of GAA may therefore increase methyl group requirements, and this may affect methyl group utilization. Our experiment evaluated the metabolic responses of growing cattle to postruminal supplementation of GAA, in a model where methionine (Met) was deficient, with and without Met supplementation. Seven ruminally cannulated Holstein steers (161 kg initial body weight [BW]) were limit-fed a soybean hull-based diet (2.7 kg/d dry matter) and received continuous abomasal infusions of an essential amino acid (AA) mixture devoid of Met to ensure that no AA besides Met limited animal performance. To provide energy without increasing the microbial protein supply, all steers received ruminal infusions of 200 g/d acetic acid, 200 g/d propionic acid, and 50 g/d butyric acid, as well as abomasal infusions of 300 g/d glucose. Treatments, provided abomasally, were arranged as a 2 × 3 factorial in a split-plot design, and included 0 or 6 g/d of l-Met and 0, 7.5, and 15 g/d of GAA. The experiment included six 10-d periods. Whole body Met flux was measured using continuous jugular infusion of 1-13C-l-Met and methyl-2H3-l-Met. Nitrogen retention was elevated by Met supplementation (P < 0.01). Supplementation with GAA tended to increase N retention when it was supplemented along with Met, but not when it was supplemented without Met. Supplementing GAA linearly increased plasma concentrations of GAA and creatine (P < 0.001), but treatments did not affect urinary excretion of GAA, creatine, or creatinine. Supplementation with Met decreased plasma homocysteine (P < 0.01). Supplementation of GAA tended (P = 0.10) to increase plasma homocysteine when no Met was supplemented, but not when 6 g/d Met was provided. Protein synthesis and protein degradation were both increased by GAA supplementation when no Met was supplemented, but decreased by GAA supplementation when 6 g/d Met were provided. Loss of Met through transsulfuration was increased by Met supplementation, whereas synthesis of Met from remethylation of homocysteine was decreased by Met supplementation. No differences in transmethylation, transsulfuration, or remethylation reactions were observed in response to GAA supplementation. The administration of GAA, when methyl groups are not limiting, has the potential to improve lean tissue deposition and cattle growth.

中文翻译：

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添加胍基乙酸对牛氮保留和蛋氨酸通量的影响

肌酸在肌肉中储存高能磷酸键，并通过胍基乙酸 (GAA) 的甲基化在肝脏中合成。因此，补充 GAA 可能会增加对甲基的需求，这可能会影响甲基的利用。我们的实验评估了生长牛对瘤后补充 GAA 的代谢反应，在一个甲硫氨酸 (Met) 缺乏的模型中，添加和不添加 Met。七头瘤胃插管荷斯坦肉牛（161 kg 初始体重 [BW]）被限制饲喂以大豆皮为基础的日粮（2.7 kg/d 干物质），并连续向厌食输注不含 Met 的必需氨基酸 (AA) 混合物以确保除了 Met 之外没有 AA 限制了动物的表现。在不增加微生物蛋白质供应的情况下提供能量，所有公牛接受瘤胃输液 200 g/d 乙酸、200 g/d 丙酸和 50 g/d 丁酸，以及 300 g/d 葡萄糖的胃液输液。在裂区设计中，以 2 × 3 因子的形式提供异常处理，包括 0 或 6 g/d 的 l-Met 和 0、7.5 和 15 g/d 的 GAA。该实验包括六个 10 天周期。使用 1-13C-1-Met 和甲基-2H3-1-Met 的连续颈静脉输注测量全身 Met 通量。Met 补充提高了氮保留（P < 0.01）。当与 Met 一起添加时，添加 GAA 往往会增加 N 保留，但在不添加 Met 时不会增加。补充 GAA 线性增加 GAA 和肌酸的血浆浓度 (P < 0.001)，但治疗不影响 GAA、肌酸或肌酸酐的尿排泄。补充 Met 降低了血浆同型半胱氨酸 (P < 0.01)。当没有补充 Met 时，GAA 的补充倾向于（P = 0.10）增加血浆同型半胱氨酸，但在提供 6 g/d Met 时则不会。当不补充 Met 时，蛋白质合成和蛋白质降解均因 GAA 补充而增加，但在提供 6 g/d Met 时，因 GAA 补充而减少。补充Met增加了通过转硫作用损失的Met，而补充Met减少了从同型半胱氨酸的再甲基化合成Met。在补充 GAA 后，未观察到转甲基化、转硫或再甲基化反应的差异。当甲基不受限制时，GAA 的施用具有改善瘦肉组织沉积和牛生长的潜力。