Wang G, Pan SJ. Microbiota-bile acid crosstalk and hepatic gluconeogenesis after intestinal resection: Revisiting the gut-liver axis for metabolic recovery. World J Gastrointest Surg 2026; 18(4): 115467 [DOI: 10.4240/wjgs.v18.i4.115467]
Corresponding Author of This Article
Gang Wang, PhD, MD, Professor, Department of General Surgery, The First Affiliated Hospital of Soochow University, No. 899 Pinghai Road, Suzhou 215006, Jiangsu Province, China. 286651551@qq.com
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Gastroenterology & Hepatology
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Editorial
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Apr 27, 2026 (publication date) through Apr 24, 2026
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Publication Name
World Journal of Gastrointestinal Surgery
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1948-9366
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Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA
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Wang G, Pan SJ. Microbiota-bile acid crosstalk and hepatic gluconeogenesis after intestinal resection: Revisiting the gut-liver axis for metabolic recovery. World J Gastrointest Surg 2026; 18(4): 115467 [DOI: 10.4240/wjgs.v18.i4.115467]
World J Gastrointest Surg. Apr 27, 2026; 18(4): 115467 Published online Apr 27, 2026. doi: 10.4240/wjgs.v18.i4.115467
Microbiota-bile acid crosstalk and hepatic gluconeogenesis after intestinal resection: Revisiting the gut-liver axis for metabolic recovery
Gang Wang, Sheng-Jie Pan
Gang Wang, Department of General Surgery, The First Affiliated Hospital of Soochow University, Suzhou 215006, Jiangsu Province, China
Sheng-Jie Pan, Department of Neurology, The First Affiliated Hospital of Soochow University, Suzhou 215006, Jiangsu Province, China
Co-corresponding authors: Gang Wang and Sheng-Jie Pan.
Author contributions: Wang G and Pan SJ contributed equally to this manuscript and are co-corresponding authors. Wang G contributed to conceptualization, interpretation of mechanistic implications, and critical revision of the manuscript; Pan SJ contributed to literature analysis, drafting of the manuscript, and integration of immunometabolic concepts; Wang G and Pan SJ contributed to data interpretation, responsibility for the accuracy and integrity of the work, approval of the final version, and agreement to be accountable for all aspects of the work.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Corresponding author: Gang Wang, PhD, MD, Professor, Department of General Surgery, The First Affiliated Hospital of Soochow University, No. 899 Pinghai Road, Suzhou 215006, Jiangsu Province, China. 286651551@qq.com
Received: October 20, 2025 Revised: November 25, 2025 Accepted: January 4, 2026 Published online: April 27, 2026 Processing time: 189 Days and 4.7 Hours
Abstract
Intestinal resection induces profound metabolic adaptations through coordinated interactions between the gut microbiota, bile acid signaling, and host endocrine pathways. In a recent study published in World Journal of Gastroenterology, Xu et al identified a Prevotellaceae_NK3B31_group-derived secondary bile acid, 7-ketolithocholic acid, as a potent activator of ileal farnesoid X receptor, linking microbial metabolism to fibroblast growth factor 19 and glucagon-like peptide-1 signaling and suppression of hepatic gluconeogenesis. This editorial highlights the significance of this microbiota-bile acid-hepatic axis within a broader immunometabolic framework. We further discuss the integration of bile acid signaling with inflammatory regulation, gut barrier integrity, and circadian metabolic control. While these findings provide important mechanistic insights, causality remains to be established, and the contribution of specific microbial taxa requires further validation. From a translational perspective, this work supports the development of microbiota-targeted interventions and pharmacologic modulation of bile acid receptors to enhance postoperative metabolic recovery. Understanding the multidomain adaptation triggered by intestinal reconstruction may enable precision strategies to improve metabolic resilience after surgery.
Core Tip: Intestinal resection reshapes systemic metabolism through coordinated microbiota-bile acid-hepatic signaling. Xu et al identified a 7-ketolithocholic acid-mediated farnesoid X receptor pathway linking microbial metabolism to suppression of hepatic gluconeogenesis. This editorial integrates these findings with broader immunometabolic and circadian mechanisms, emphasizing the role of bile acid signaling in postoperative metabolic adaptation. These insights highlight potential strategies for microbiota-targeted and receptor-based interventions to enhance metabolic recovery after surgery.
