张厦, 袁斌, 陈晓斌. 儿童迁延性泄泻脾阳虚证的粪便代谢组学研究[J]. 南京中医药大学学报, 2024, 40(6): 633-639. DOI: 10.14148/j.issn.1672-0482.2024.0633
引用本文: 张厦, 袁斌, 陈晓斌. 儿童迁延性泄泻脾阳虚证的粪便代谢组学研究[J]. 南京中医药大学学报, 2024, 40(6): 633-639. DOI: 10.14148/j.issn.1672-0482.2024.0633
ZHANG Sha, YUAN Bin, CHEN Xiaobin. Fecal Metabolomics Study of Persistent Diarrhea with Spleen Yang Deficiency Syndrome[J]. Journal of Nanjing University of traditional Chinese Medicine, 2024, 40(6): 633-639. DOI: 10.14148/j.issn.1672-0482.2024.0633
Citation: ZHANG Sha, YUAN Bin, CHEN Xiaobin. Fecal Metabolomics Study of Persistent Diarrhea with Spleen Yang Deficiency Syndrome[J]. Journal of Nanjing University of traditional Chinese Medicine, 2024, 40(6): 633-639. DOI: 10.14148/j.issn.1672-0482.2024.0633

儿童迁延性泄泻脾阳虚证的粪便代谢组学研究

Fecal Metabolomics Study of Persistent Diarrhea with Spleen Yang Deficiency Syndrome

  • 摘要:
      目的  从粪便代谢角度探寻儿童迁延性泄泻脾阳虚证的证候物质基础。
      方法  选取20例脾阳虚证的迁延性泄泻患儿作为观察组,20例健康儿童作为对照组,采集各组的粪便样本后,采用气相色谱质谱联用仪器对样本进行代谢组学分析,比较2组代谢物的差异。
      结果  与儿童迁延性泄泻脾阳虚证相关的潜在生物标志物有25种,在迁延性泄泻脾阳虚证患儿的粪便中下调的有9种代谢物,分别为L-谷氨酰胺、L-谷氨酸、4-羟基苯甲醛、L-半胱氨酸、鸟氨酸、L-异亮氨酸、丁二酸、β-丙氨酸、富马酸,在泄泻脾阳虚证患儿的粪便中上调的有16种代谢物,包括丝氨酸、核糖酸、α-亚麻酸、苯甲酸、果糖、L-丙氨酸、焦谷氨酸、丙酮酸、次黄嘌呤、癸酸、L-天门冬氨酸等代谢物,涉及相关通路有7条,包括丙氨酸、天冬氨酸和谷氨酸代谢、D-谷氨酰胺和D-谷氨酸代谢、丙酮酸代谢、精氨酸和脯氨酸代谢、精氨酸生物合成、糖酵解/糖异生、柠檬酸循环(TCA循环)。
      结论  迁延性泄泻脾阳虚证患儿与健康儿童相比,神经调节代谢发生紊乱,能量代谢发生异常,机体无氧酵解有所增强,相关差异代谢物的发现可能对儿童迁延性泄泻脾阳虚证的发病机制、诊断和治疗均奠定了一定的物质基础。

     

    Abstract:
      OBJECTIVE  To explore the syndrome material basis of spleen yang deficiency syndrome in children with diarrhea from the perspective of fecal metabolism.
      METHODS  20 children with persistent diarrhea of spleen yang deficiency syndrome were selected as the observation group, and 20 healthy children were selected as the normal control group. After collecting the fecal samples of each group, the samples were analyzed by gas chromatography-mass spectrometry, and the differences in metabolites between the two groups were compared.
      RESULTS  There were 25 potential biomarkers related to persistent diarrhea with spleen yang deficiency syndrome, among which 9 were down-regulated, namely L-glutamine, L-Glutamic acid, 4-hydroxybenzaldehyde, L-cysteine, ornithine, L-isoleucine, succinic acid, β-alanine, fumaric acid, in persistent diarrhea with spleen yang deficiency syndrome. There were 16 kinds of upregulation in the stool of children, including serine, ribonic acid, α-linolenic acid, benzoic acid, fructose, L-alanine, pyroglutamic acid, pyruvate, hypoxanthine, capric acid, L-aspartic acid, and other metabolites. There were 7 related pathways involved, including the metabolism of alanine, aspartic acid and glutamate, the metabolism of D-glutamine and D-glutamate, the metabolism of pyruvate, the metabolism of arginine and proline, arginine biosynthesis, glycolysis/gluconeogenesis, citric acid cycle (TCA cycle).
      CONCLUSION  Compared with healthy children, children with persistent diarrhea with spleen yang deficiency syndrome may experience disturbances in neural regulation metabolism, abnormal energy metabolism, and enhanced anaerobic fermentation in the body. The discovery of related differential metabolites may lay a certain material foundation for the pathogenesis, diagnosis, and treatment of persistent diarrhea with spleen yang deficiency syndrome in children.

     

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