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魔芋葡甘聚糖对便秘小鼠胃、小肠和大肠代谢物的影响及 KEGG 通路预测。

Effect of konjac glucomannan on metabolites in the stomach, small intestine and large intestine of constipated mice and prediction of the KEGG pathway.

机构信息

College of Food Science, Southwest University, Chongqing 400715, China.

出版信息

Food Funct. 2021 Apr 7;12(7):3044-3056. doi: 10.1039/d0fo02682d. Epub 2021 Mar 12.

Abstract

The occurrence of constipation involves the whole gastrointestinal tract. Konjac glucomannan (KGM) has been clinically proven to alleviate constipation, but its mechanism has not been fully understood. The present study aimed to investigate the excretion-promoting effect of KGM on constipated mice and the underlying molecular mechanism. In this study, the UHPLC-QE orbitrap/MS method was used to determine the metabolic phenotypes of total gastrointestinal segments (i.e., the stomach {St}, small intestine {S}, and large intestine {L}) in constipated mice treated with KGM. The results showed that KGM improved the fecal water content, body weight growth rate, and serum gastrointestinal regulation related peptide levels. The metabolomics results revealed the decreased levels of amino acids, cholines, deoxycholic acid, arachidonic acid, thiamine and the increased levels of indoxyl sulfate, histamine, linoelaidic acid etc. The KEGG pathway analysis indicated that the relaxation effect of KGM supplementation was most likely driven by modulating the expression levels of various key factors involved in biosynthesis of amino acid (i.e., phenylalanine, tyrosine and tryptophan), linoleic acid metabolism, biosynthesis of secondary metabolites, and arachidonic acid metabolism signalling pathways. The results indicated that KGM alleviates constipation by regulating potential metabolite markers and metabolic pathways in different gastrointestinal segments.

摘要

便秘的发生涉及整个胃肠道。魔芋葡甘聚糖(KGM)已被临床证明可缓解便秘,但其机制尚未完全阐明。本研究旨在探讨 KGM 对便秘小鼠的促排泄作用及其潜在的分子机制。在这项研究中,我们使用 UHPLC-QE orbitrap/MS 方法来确定 KGM 处理后便秘小鼠整个胃肠道段(即胃{St}、小肠{S}和大肠{L})的代谢表型。结果表明,KGM 可改善粪便含水量、体重增长率和血清胃肠调节相关肽水平。代谢组学结果显示,氨基酸、胆碱、脱氧胆酸、花生四烯酸、硫胺素的水平降低,而吲哚硫酸、组氨酸、亚油酸等的水平升高。KEGG 途径分析表明,KGM 补充剂的松弛作用可能是通过调节参与氨基酸(即苯丙氨酸、酪氨酸和色氨酸)、亚油酸代谢、次生代谢物生物合成和花生四烯酸代谢信号通路的各种关键因子的表达水平来驱动的。结果表明,KGM 通过调节不同胃肠道段的潜在代谢标志物和代谢途径来缓解便秘。

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