D-mannose, essential for protein glycosylation, has been reported to have immunomodulatory effects and to maintain intestinal flora homeostasis. In addition to evaluating growth performance, we examined the impact of D-mannose on the structure of epithelial cells and apical junction complexes in the animal intestine. All 1800 grass carp (16.20 ± 0.01 g) were randomly divided into six treatments with six replicates of 50 fish each and fed with six different levels of D-mannose (0.52, 1.75, 3.02, 4.28, 5.50 and 6.78 g/kg diet) for 70 d. The study revealed that D-mannose increased feed intake (P < 0.001) but did not affect the percent weight gain (PWG), special growth rate, and feed conversion ratio (P > 0.05). D-mannose supplementation at 1.75 g/kg increased crude protein content in fish and lipid production value (P < 0.05). D-mannose supplementation at 4.28 g/kg increased intestinal length, intestinal weight and fold height of grass carp compared to the control group (P < 0.05). This improvement may be attributed to the phosphomannose isomerase (PMI)-mediated enhancement of glycolysis. This study found that D-mannose supplementation at 4.28 or 3.02 g/kg reduced serum diamine oxidase activity or D-lactate content (P < 0.05) and improved cellular and intercellular structures for the first time. The improvement of cellular redox homeostasis involves alleviating endoplasmic reticulum (ER) stress through the inositol-requiring enzyme 1 (IRE1), RNA-dependent protein kinase-like ER kinase (PERK), and activating transcription factor 6 (ATF6) signaling pathways. The alleviation of ER stress may be linked to the phosphomannomutase (PMM)-mediated enhancement of protein glycosylation. In addition, ubiquitin-dependent [PTEN-induced putative kinase 1 (PINK1)/Parkin] and ubiquitin-independent [BCL2-interacting protein 3-like (BNIP3L), BCL2-interacting protein 3 (BNIP3), and FUN14 domain containing 1 (FUNDC1)] mitophagy may play a role in maintaining cellular redox homeostasis. The enhancement of intercellular structures includes enhancing tight junction and adherent junction structures, which may be closely associated with the small Rho GTPase protein (RhoA)/the Rho-associated protein kinase (ROCK) signaling pathway. In conclusion, D-mannose improved intestinal cellular redox homeostasis associated with ER stress and mitophagy pathways, and enhanced intercellular structures related to tight junctions and adherent junctions. Furthermore, quadratic regression analysis of the PWG and intestinal reactive oxygen species content indicated that the optimal addition level of D-mannose for juvenile grass carp was 4.61 and 4.59 g/kg, respectively.

中文翻译：

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建立 D-甘露糖与幼鱼草鱼 （Ctenopharyngodon idella） 之间的联系：与内质网应激、线粒体自噬和顶端交界复合体相关的生长和肠道结构改善


D-甘露糖是蛋白质糖基化所必需的，据报道具有免疫调节作用并维持肠道菌群稳态。除了评估生长性能外，我们还检查了 D-甘露糖对动物肠道上皮细胞和顶端连接复合物结构的影响。将所有 1800 条草鱼 （16.20 ± 0.01 g） 随机分为 6 个处理，每个处理 6 个重复，每个 50 条鱼，并投喂 6 个不同水平的 D-甘露糖 （0.52、1.75、3.02、4.28、5.50 和 6.78 g/kg 日粮） 70 d。研究表明，D-甘露糖增加了采食量 （P < 0.001），但不影响增重百分比 （PWG）、特殊生长速率和饲料转化率 （P > 0.05）。添加 1.75 g/kg 的 D-甘露糖增加了鱼中的粗蛋白含量和脂质生产值 （P < 0.05）。与对照组相比，添加 4.28 g/kg 的 D-甘露糖可增加草鱼的肠道长度、肠道重量和褶皱高度 （P < 0.05）。这种改善可能归因于磷酸甘露糖异构酶 （PMI） 介导的糖酵解增强。本研究发现，添加 4.28 或 3.02 g/kg 的 D-甘露糖可降低血清二胺氧化酶活性或 D-乳酸含量 （P < 0.05），并首次改善细胞和细胞间结构。细胞氧化还原稳态的改善包括通过肌醇需求酶 1 （IRE1）、RNA 依赖性蛋白激酶样 ER 激酶 （PERK） 和激活转录因子 6 （ATF6） 信号通路缓解内质网 （ER） 应激。ER 应激的缓解可能与磷酸甘露糖变位酶 （PMM） 介导的蛋白质糖基化增强有关。 此外，泛素依赖性 [PTEN 诱导的推定激酶 1 （PINK1）/Parkin] 和泛素非依赖性 [BCL2 相互作用蛋白 3 样 （BNIP3L）、BCL2 相互作用蛋白 3 （BNIP3） 和包含 1 的 FUN14 结构域 （FUNDC1）] 线粒体自噬可能在维持细胞氧化还原稳态中发挥作用。细胞间结构的增强包括增强紧密连接和粘附连接结构，这可能与小 Rho GTP 酶蛋白 （RhoA）/Rho 相关蛋白激酶 （ROCK） 信号通路密切相关。总之，D-甘露糖改善了与 ER 应激和线粒体自噬途径相关的肠道细胞氧化还原稳态，并增强了与紧密连接和粘附连接相关的细胞间结构。此外，PWG 和肠道活性氧含量的二次回归分析表明，草鱼幼鱼 D-甘露糖的最佳添加量分别为 4.61 和 4.59 g/kg。