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肠道微生物群参与并重塑宿主代谢:从治疗患者到治疗其肠道菌群。

Gut microbiota participates and remodels host metabolism: From treating patients to treating their gut flora.

作者信息

Han Shuang, Li Rui-Hua, Gao Peng

机构信息

Department of Clinical Laboratory, The Second Affiliated Hospital of Dalian Medical University, Dalian 116023, Liaoning Province, China.

出版信息

World J Gastroenterol. 2024 Dec 7;30(45):4839-4843. doi: 10.3748/wjg.v30.i45.4839.

DOI:10.3748/wjg.v30.i45.4839
PMID:39649550
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11606374/
Abstract

In this editorial, we comment on Liu s article published in the recent issue of the . Biochemically and pathologically, Liu proved that the urate-lowering activity of leech total protein (LTP) was mainly attributed to the rectification of gut microbiota. Specifically, we noticed the change in and after LTP administration. Both bacteria have been reported to alleviate metabolic dysfunction-associated steatohepatitis and other chronic metabolic diseases. LTP was administrated through intragastric manners. Most possibly, LTP would be digested by the gut microbiota further. The anti-hyperuricemia effects should, to the most possible extent, be exerted by the peptides or their secondary metabolic products. Human gut microbiota communicates with other organs through metabolites generated by the microbes or co-metabolized with the host. Whether the anti-hyperuricemia effect could be partially ascribed to the microbiota metabolites also deserves to be discussed. Although metabolomics analysis was performed for serum samples, fecal metabolomics was highly advocated which could facilitate exact mechanism explanation. This study implied that gut microbiota contains many unexplored targets with different therapeutic potentials. It is foreseeable that utilizing these targets can avoid the impairment or side effects of directly using human targets to some extent.

摘要

在这篇社论中,我们对刘最近发表在《[期刊名称]》上的文章进行评论。从生化和病理角度来看,刘证明了水蛭总蛋白(LTP)的降尿酸活性主要归因于肠道微生物群的调节。具体而言,我们注意到给予LTP后[两种细菌名称]的变化。据报道,这两种细菌都能减轻代谢功能障碍相关的脂肪性肝炎和其他慢性代谢疾病。LTP通过胃内给药方式给予。很可能,LTP会被肠道微生物群进一步消化。抗高尿酸血症作用应尽可能由肽或其次级代谢产物发挥。人体肠道微生物群通过微生物产生的代谢产物或与宿主共同代谢的产物与其他器官进行交流。抗高尿酸血症作用是否能部分归因于微生物群代谢产物也值得探讨。尽管对血清样本进行了代谢组学分析,但强烈提倡进行粪便代谢组学分析,这有助于准确解释机制。这项研究表明肠道微生物群包含许多具有不同治疗潜力且尚未被探索的靶点。可以预见,利用这些靶点在一定程度上可以避免直接作用于人体靶点所带来的损害或副作用。

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Plasma sphingolipids mediate the association between gut microbiome composition and type 2 diabetes risk in the HELIUS cohort: a case-cohort study.血浆神经酰胺介导肠道微生物群组成与 HELIUS 队列 2 型糖尿病风险之间的关联:病例-队列研究。
BMJ Open Diabetes Res Care. 2024 Jul 18;12(4):e004180. doi: 10.1136/bmjdrc-2024-004180.
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The pathogenesis of gout: molecular insights from genetic, epigenomic and transcriptomic studies.痛风的发病机制:来自遗传、表观基因组和转录组学研究的分子见解
Nat Rev Rheumatol. 2024 Aug;20(8):510-523. doi: 10.1038/s41584-024-01137-1. Epub 2024 Jul 11.
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