The purpose of this study was to gain insight into the mechanism of iron dextran (DexFe) absorption in the intestines. A total of 72 piglets (average BW = 7.12 ± 0.75 kg, male to female ratio = 1:1) weaned at 28 d of age were randomly divided into two treatment groups with six replicates for each group. The experimental diets included the basal diet supplemented with 100 mg/kg iron dextran (DexFe group) and the basal diet supplemented with 100 mg/kg FeSO4·H2O (CON group). The experiment lasted for 28 d. The piglets' intestinal iron transport was measured in vitro using an Ussing chamber. Porcine intestinal epithelial cell line (IPEC-J2) cells were used to develop a monolayer cell model that explored the molecular mechanism of DexFe absorption. Results showed that compared to the CON group, the ADG of pigs in the DexFe group was improved (P = 0.022), while the F/G was decreased (P = 0.015). The serum iron concentration, apparent iron digestibility, and iron deposition in the duodenum, jejunum, and ileum were increased (P < 0.05) by dietary DexFe supplementation. Piglets in the DexFe group had higher serum red blood count, hemoglobin, serum iron content, serum ferritin and transferrin levels and lower total iron binding capacity (P < 0.05). In the Ussing chamber test, the iron absorption rate of the DexFe group was greater (P < 0.001) than the CON group, and there was no significant difference between the DexFe group and the glucose group (P > 0.05). Furthermore, when compared to the CON group, DexFe administration improved (P < 0.05) SLC2A5 gene and glucose transporter 5 (GLUT5) protein expression but had no effect (P > 0.05) on SLC11A2 gene or divalent metal transporter 1 (DMT1) protein expression. Once the GLUT5 protein was suppressed, the iron transport rate and apparent permeability coefficient were decreased (P < 0.05) in IPEC-J2 monolayer cell models. The findings suggest the effectiveness of DexFe application in weaned piglets and revealed for the first time that DexFe absorption in the intestine is closely related to the glucose transporter GLUT5 protein channel.

中文翻译：

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铁吸收机制的新见解：通过葡萄糖转运蛋白 5 （GLUT5） 和二价金属转运蛋白 1 （DMT1） 转运蛋白在断奶仔猪肠道中摄取右旋糖酐铁


本研究的目的是深入了解右旋糖酐铁 （DexFe） 在肠道中的吸收机制。将 72 头在 28 d 时断奶的仔猪 （平均体重 = 7.12 ± 0.75 kg，雄母比 = 1：1） 随机分为两个处理组，每组 6 个重复。实验日粮包括添加 100 mg/kg 右旋糖酐铁的基础日粮（DexFe 组）和添加 100 mg/kg FeSO4· 的基础日粮H2O （CON 组）。实验持续 28 d。使用 Ussing 室在体外测量仔猪的肠道铁运输。采用猪肠上皮细胞系 （IPEC-J2） 细胞构建单层细胞模型，探讨 DexFe 吸收的分子机制。结果显示，与 CON 组相比，DexFe 组猪的 ADG 有所提高 （P = 0.022），而 F/G 降低 （P = 0.015）。膳食补充 DexFe 可增加血清铁浓度、表观铁消化率和十二指肠、空肠和回肠中的铁沉积 （P < 0.05）。DexFe 组仔猪血清红细胞计数、血红蛋白、血清铁含量、血清铁蛋白和转铁蛋白水平较高，总铁结合力较低 （P < 0.05）。Ussing chamber 试验中，DexFe 组的铁吸收率 （P < 0.001） 大于 CON 组，DexFe 组与葡萄糖组差异无统计学意义 （P > 0.05）。此外，与 CON 组相比，DexFe 给药改善了 （P < 0.05） SLC2A5 基因和葡萄糖转运蛋白 5 （GLUT5） 蛋白表达，但对 SLC11A2 基因或二价金属转运蛋白 1 （DMT1） 蛋白表达没有影响 （P > 0.05）。 一旦 GLUT5 蛋白被抑制，IPEC-J2 单层细胞模型中铁转运速率和表观渗透系数降低 （P < 0.05）。研究结果表明 DexFe 在断奶仔猪中的应用的有效性，并首次揭示了 DexFe 在肠道中的吸收与葡萄糖转运蛋白 GLUT5 蛋白通道密切相关。