Decreased intake is induced by stressors such as parturition, transportation, dietary transitions, and disease. An important function of one-carbon metabolism (OCM) is to produce the antioxidant glutathione to help reduce oxidative stress. Although various components of OCM are expressed in the bovine rumen and small intestine, the relationship between reduced feed intake, OCM, and antioxidant mechanisms in gut tissues is unknown. This study aimed to assess alterations in immune and antioxidant pathways in ruminal epithelium due to acute feed restriction (FR). Seven group-housed ruminally cannulated Angus steers (663 ± 73 kg body weight, 2 yr old) had ad libitum access to a finishing diet (dry-rolled corn, corn silage, modified wet distiller’s grains) during 15 d of a pre-FR period (PRE). Subsequently, steers were moved to a metabolism barn with tie stalls and individually fed at 25% of estimated intake in PRE for 3 d (FR period, FRP). This was followed by 15 d of recovery (POST) during which steers had ad libitum access to the same diet as in PRE and FRP. Plasma and ruminal tissue biopsies were collected during each period. Plasma free fatty acid and IL1-β concentrations were higher (P ≤ 0.03) in FRP than PRE or POST. The mRNA abundance of the proinflammatory genes tumor necrosis factor, toll-like receptor 2 (TLR2), and TLR4 in the ruminal epithelium peaked (P < 0.05) at FRP and remained higher at POST. These responses agreed with the higher (P < 0.05) abundance of phosphorylated (p)-MAPK (an inflammation activator) and p-EEF2 (translational repressor) in FRP than PRE and POST. Although ruminal glutathione peroxidase (GPX) enzyme activity did not increase at FRP compared with PRE and POST, protein abundance of GPX1 and GPX3 along with the antioxidant response regulator NFE2L2 were highest (P < 0.01), and the activity of cystathionine-beta synthase tended (P = 0.06) to be highest during FR. Although FR had minimal negative effects on tissue integrity-related genes (only filamin A was downregulated), it led to a systemic inflammatory response and triggered inflammation and antioxidant mechanisms within the ruminal epithelium. Thus, deploying anti-inflammatory and antioxidant mechanisms via molecules that feed into OCM (e.g., dietary methyl donors such as methionine, choline, betaine, and folate) could potentially counteract the stressors associated with FR.

中文翻译：

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短期限食通过安格斯阉牛瘤胃上皮中的胱硫醚-β-合酶和谷胱甘肽过氧化物酶诱导炎症和抗氧化反应


摄入量减少是由压力源引起的，例如分娩、运输、饮食转变和疾病。一碳代谢 （OCM） 的一个重要功能是产生抗氧化剂谷胱甘肽，以帮助减少氧化应激。尽管 OCM 的各种成分在牛瘤胃和小肠中表达，但采食量减少、OCM 和肠道组织中抗氧化机制之间的关系尚不清楚。本研究旨在评估急性喂养限制 （FR） 引起的瘤胃上皮免疫和抗氧化途径的改变。7 头群养反刍空管安格斯公牛 （663 ± 73 kg 体重，2 岁） 在 FR 前 （PRE） 的 15 d 内随意进行育肥饲料 （干轧玉米、玉米青贮饲料、改良湿酒糟）。随后，将阉牛转移到带有系带栏的新陈代谢牛舍，并以 PRE 估计摄入量的 25% 单独饲喂 3 天 （FR 期，FRP）。随后是 15 天的恢复 （POST），在此期间，阉牛可以随意获得与 PRE 和 FRP 相同的饮食。在每个时期收集血浆和瘤胃组织活检。FRP 中的血浆游离脂肪酸和 IL1-β 浓度高于 PRE 或 POST （P ≤ 0.03）。瘤胃上皮促炎基因肿瘤坏死因子、toll样受体 2 （TLR2） 和 TLR4 的 mRNA 丰度在 FRP 时达到峰值 （P < 0.05），在 POST 时保持较高。这些反应与 FRP 中磷酸化 （p）-MAPK （一种炎症激活剂） 和 p-EEF2 （翻译抑制因子） 的丰度高于 PRE 和 POST 一致 （P < 0.05）。 虽然与 PRE 和 POST 相比，FRP 的瘤胃谷胱甘肽过氧化物酶 （GPX） 酶活性没有增加，但 GPX1 和 GPX3 以及抗氧化反应调节因子 NFE2L2 的蛋白质丰度最高 （P < 0.01），胱硫醚-β 合酶的活性趋于 （P = 0.06） 在 FR 期间最高。尽管 FR 对组织完整性相关基因的负面影响最小 （只有细丝蛋白 A 下调），但它导致全身炎症反应并触发瘤胃上皮内的炎症和抗氧化机制。因此，通过馈入 OCM 的分子（例如，膳食甲基供体，如蛋氨酸、胆碱、甜菜碱和叶酸）部署抗炎和抗氧化机制可能会抵消与 FR 相关的压力源。