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首页> 外文期刊>The Journal of Nutritional Biochemistry >Lactoferrin up-regulates intestinal gene expression of brain-derived neurotrophic factors BDNF, UCHL1 and alkaline phosphatase activity to alleviate early weaning diarrhea in postnatal piglets
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Lactoferrin up-regulates intestinal gene expression of brain-derived neurotrophic factors BDNF, UCHL1 and alkaline phosphatase activity to alleviate early weaning diarrhea in postnatal piglets

机译：乳铁蛋白上调脑源性神经营养因子BDNF，UCHL1和碱性磷酸酶活性的肠道基因表达，以减轻出生后仔猪的早期断奶腹泻

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摘要

The molecular mechanisms underlying how dietary lactoferrin (Lf) impacts gut development and maturation and protects against early weaning diarrhea are not well understood. In this study, we supplemented postnatal piglets with an Lf at a dose level of 155 and 285 mg/kg/day from 3 to 38 days following birth. Our findings show that the high dose of Lf up-regulated messenger RNA expression levels of genes encoding brain-derived neurotrophic factor (BDNF) and ubiquitin carboxy-terminal hydrolase L1 (ubiquitin thiolesterase (UCHL1) and, to a lesser extent, glial cell line-derived neurotrophic factor, in the duodenum (P.05). Piglets in the high and low Lf group had 30% and 7% larger jejunal crypts compared with the control group (P.05). Escherichia coli 16S rRNA copy number per gram of ascending colon contents was significantly reduced (P=.001), while the copy number of Bifidobacteria and Lactobacillus spp. was not affected. In addition, Lf increased intestinal alkaline phosphatase activity (P.05) and delayed the onset of food transitional diarrhea, reducing its frequency and duration (P.05). The incidence of diarrhea in the high and low Lf groups was decreased 54% and 15%, respectively, compared with the control group (P=.035). In summary, these findings provide new evidence that dietary Lf supplementation up-regulated gene expression of BDNF and UCHL1, decreased the colon microbiota of E. coli, improved gut maturation and reduced early weaning diarrhea in piglets. The molecular basis underlying these findings suggests that Lf may enhance gut development and immune function by providing new insight into the gut-brain-microbe axis that has not been previously reported. (C) 2014 Elsevier Inc. All rights reserved.
机译：饮食中的乳铁蛋白（Lf）如何影响肠道发育和成熟并防止早期断奶腹泻的分子机制尚不清楚。在这项研究中，我们在出生后3至38天以155和285 mg / kg / day的剂量补充Lf给产后仔猪。我们的研究结果表明，高剂量的Lf上调了编码脑源性神经营养因子（BDNF）和泛素羧基末端水解酶L1（泛素硫酯酶（UCHL1））的基因的信使RNA表达水平，并在较小程度上影响了神经胶质细胞系十二指肠中的神经营养因子（P <.05）。高和低Lf组的仔猪空肠隐窝比对照组（P <.05）分别大30％和7％。大肠杆菌16S rRNA拷贝数每克上升结肠含量显着降低（P = .001），而双歧杆菌和乳杆菌属的拷贝数不受影响;此外，Lf增加肠道碱性磷酸酶活性（P <.05）并延迟了发病时间。食物过渡性腹泻，减少了腹泻的发生频率和持续时间（P <.05），与对照组相比，高和低Lf组的腹泻发生率分别降低了54％和15％（P = .035）。综上所述，这些发现为饮食L提供了新的证据。 f补充上调BDNF和UCHL1的基因表达，减少大肠杆菌的结肠菌群，改善肠道成熟并减少仔猪的早期断奶腹泻。这些发现的分子基础表明，Lf可以通过提供对肠道-脑-微生物轴的新见解来增强肠道的发育和免疫功能，而此前尚未有报道。 （C）2014 Elsevier Inc.保留所有权利。

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