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Copyright: ©Author(s) 2026. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution-NonCommercial (CC BY-NC 4.0) license. No commercial re-use. See permissions. Published by Baishideng Publishing Group Inc.
World J Hepatol. May 27, 2026; 18(5): 115514
Published online May 27, 2026. doi: 10.4254/wjh.v18.i5.115514
Letter to the Editor: Gut microbiota–bile acid crosstalk - Prevotellaceae NK3B31 and 7-ketolithocholic acid drive metabolic benefits of distal bowel resection with preservation of terminal ileum
Chao-Ming Zhou, Zheng Liang, Liu Chen, Bing-Qian Yin, Long-Yao Xu, Xu Cui
Xu Cui, Long-Yao Xu, Bing-Qian Yin, Liu Chen, Zheng Liang, Chao-Ming Zhou, Department of Pediatric Surgery, Fujian Children’s Hospital (Fujian Branch of Shanghai Children’s Medical Center), College of Clinical Medicine for Obstetrics & Gynecology and Pediatrics, Fujian Medical University, Fuzhou 350014, Fujian Province, China
Zheng Liang, Institute of Transformation Studies, Fujian Children’s Hospital (Fujian Branch of Shanghai Children’s Medical Center), Fuzhou 350001, Fujian Province, China
Co-first authors: Xu Cui and Long-Yao Xu.
Co-corresponding authors: Liu Chen and Chao-Ming Zhou.
Author contributions: Cui X conceived the core idea of the letter, drafted the initial manuscript, conducted a systematic literature review on gut microbiota–bile acid crosstalk and metabolic surgery mechanisms, and led the analysis of 7-KLCA-related signaling pathways; Xu LY contributed equally to manuscript drafting, participated in the construction of the mechanistic framework for the Prevotellaceae_NK3B31_group-7-KLCA-FXR axis, clarified translational implications, and revised the manuscript for academic rigor; Yin BQ assisted in literature collection and verification, especially regarding microbial metabolite modification of bile acids, and provided critical comments on the clinical generalizability section; Chen L participated in the discussion of open questions, supplemented the latest research progress on GLP-1-FXR crosstalk, and optimized the logical structure of the manuscript; Liang Z verified the accuracy of molecular biology terminology and reference formatting and contributed to revising the section titled “Mechanisms linking microbial modulation to systemic bile acid signaling.” Zhou CM supervised the overall research direction, critically revised the manuscript, finalized the content, and was responsible for submission and communication with the editorial board; all authors have read and approved the final version of the manuscript. Chen L and Zhou CM contributed equally as co-corresponding authors to this letter; Chen L conceived the study, designed the experiments, performed data analysis, and drafted the manuscript; Zhou CM provided clinical guidance, supervised the research, and critically revised the manuscript for important intellectual content; Both authors approved the final version of the letter and agree to be accountable for all aspects of the work.
Supported by the Fujian Provincial Science and Technology Innovation Joint Fund Project (No. 2024Y9555), the Fujian Provincial Natural Science Foundation Project (No. 2025J01226), the Fujian Provincial Medical Project for Creating Dual High-Quality Development (High Level and High Standard; No. ETK2025004), and the Fujian Medical University Qihang Fund (No. 2023QH1239).
Conflict-of-interest statement: All authors declare that they have no conflict of interest to disclose.
Corresponding author: Chao-Ming Zhou, Department of Pediatric Surgery, Fujian Children’s Hospital (Fujian Branch of Shanghai Children’s Medical Center), College of Clinical Medicine for Obstetrics & Gynecology and Pediatrics, Fujian Medical University, No. 966 Hengyu Road, Fuzhou 350014, Fujian Province, China. fjsetyyzcm@163.com
Received: October 20, 2025
Revised: December 2, 2025
Accepted: January 7, 2026
Published online: May 27, 2026
Processing time: 220 Days and 0 Hours
Abstract

This letter commends on the study published in World Journal of Gastroenterology by Xu et al, which elucidated the mechanism by which distal bowel resection with terminal ileum preservation (DBRPI) improves hepatic gluconeogenesis via the Prevotellaceae NK3B31_group/7-ketolithocholic acid (7-KLCA)/farnesoid X receptor (FXR) axis. Using multiomics and functional assays, Xu et al identified this microbial–bile acid (BA) axis as central to the metabolic benefits of DBRPI, linking microbial enrichment (e.g., Prevotellaceae NK3B31_group) to increased 7-KLCA levels and FXR activation, thereby suppressing gluconeogenic gene expression. We highlight the novelty of this work in its focus on taxon-specific microbial and BA dynamics, which advances the understanding of postoperative glucose regulation. Additionally, we note its translational potential—targeting this axis via probiotics or 7-KLCA analogs—and raise several open questions, including causal validation of the microbial taxon, serum 7-KLCA dynamics, and glucagon-like-peptide-1/FXR interplay. Overall, this study bridges gut microbiota and BA crosstalk, offering actionable insights for the treatment of metabolic disease.

Keywords: Distal bowel resection with terminal ileum preservation; Gut microbiota; Bile acid metabolism; Prevotellaceae NK3B31_group; 7-ketolithocholic acid; Glucose homeostasis

Core Tip: Xu et al revealed that the Prevotellaceae NK3B31_group/7-ketolithocholic acid (7-KLCA)/farnesoid X receptor (FXR) axis drives suppression of hepatic gluconeogenesis in distal bowel resection with terminal ileum preservation, a metabolic surgery model. Multiomics analyses linked microbial enrichment to elevated 7-KLCA levels and FXR activation, leading to downregulation of gluconeogenic genes. This work advances the understanding of gut microbiota–bile acid crosstalk, highlighting species-specific roles of bile acids. Its translational potential lies in targeting this axis—via probiotics or 7-KLCA analogs—for the treatment of metabolic disease.

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