Letter to the Editor
Copyright ©The Author(s) 2024. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Dec 7, 2024; 30(45): 4839-4843
Published online Dec 7, 2024. doi: 10.3748/wjg.v30.i45.4839
Gut microbiota participates and remodels host metabolism: From treating patients to treating their gut flora
Shuang Han, Rui-Hua Li, Peng Gao
Shuang Han, Rui-Hua Li, Peng Gao, Department of Clinical Laboratory, The Second Affiliated Hospital of Dalian Medical University, Dalian 116023, Liaoning Province, China
Co-first authors: Shuang Han and Rui-Hua Li.
Author contributions: Han S and Li RH contributed to the writing, and editing of the manuscript, illustrations, and literature review; Gao P designed the overall manuscript concept and outline, read and approved the final manuscript; Li RH contributed to the manuscript discussion and design.
Conflict-of-interest statement: The authors declare that they have no conflicts of interest.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Peng Gao, PhD, Executive Director, Professor, Department of Clinical Laboratory, The Second Affiliated Hospital of Dalian Medical University, No. 467 Zhongshan Road, Dalian 116023, Liaoning Province, China. gaop@dmu.edu.cn
Received: July 29, 2024
Revised: September 15, 2024
Accepted: October 29, 2024
Published online: December 7, 2024
Processing time: 107 Days and 8.7 Hours
Abstract

In this editorial, we comment on Liu et al’s article published in the recent issue of the World Journal of Gastroenterology. Biochemically and pathologically, Liu et al 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 Bacteroides and Akkermansia 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.

Keywords: Gut microbiota; Metabolism; Metabolomics; Hyperuricemia; Peptides

Core Tip: In this article, we comment on Liu et al’s article about intragastric administration of leech total protein could modulate gut microbiota and alleviate hyperuricemia. We speculated that the digestive peptides either generated by the gut flora or by the host digestive system might contribute to the gut microbiota reshaping. Specifically, the study implied that gut microbiota contains many unexplored targets with different therapeutic potentials. If a drug target is developed based on the gut microbiota, it will circumvent the unwanted effects of direct human target utilization. This drug target development notion change will revolutionize the traditional disease-treating paradigm.