Abdelwahab MM, Ghattas AS, Tawheed A. Implications of gut microbiota in hepatic and pancreatic diseases: Gut-liver-pancreas axis. World J Hepatol 2025; 17(9): 109965 [DOI: 10.4254/wjh.v17.i9.109965]
Corresponding Author of This Article
Ahmed Tawheed, Department of Gastroenterology, Al Emadi Hospital, D Ring Road, Doha 50000, Qatar. atawheed1990@gmail.com
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Editorial
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (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: http://creativecommons.org/licenses/by-nc/4.0/
World J Hepatol. Sep 27, 2025; 17(9): 109965 Published online Sep 27, 2025. doi: 10.4254/wjh.v17.i9.109965
Implications of gut microbiota in hepatic and pancreatic diseases: Gut-liver-pancreas axis
Maya Magdy Abdelwahab, Ahmad S Ghattas, Ahmed Tawheed
Maya Magdy Abdelwahab, Ahmad S Ghattas, Faculty of Medicine, Helwan University, Cairo 11795, Al Qāhirah, Egypt
Ahmed Tawheed, Department of Gastroenterology, Al Emadi Hospital, Doha 50000, Qatar
Author contributions: Tawheed A designed and revised the manuscript; Abdelwahab MM and Ghattas AS wrote the manuscript.
Conflict-of-interest statement: The authors declare that they have no conflict 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: Ahmed Tawheed, Department of Gastroenterology, Al Emadi Hospital, D Ring Road, Doha 50000, Qatar. atawheed1990@gmail.com
Received: May 27, 2025 Revised: June 30, 2025 Accepted: August 12, 2025 Published online: September 27, 2025 Processing time: 121 Days and 23.8 Hours
Abstract
The gut–liver-pancreas axis (GLPA) is a critical network shaped by gut microbiota (GM) and their metabolites, essential for maintaining metabolic and immune balance. Disruption of this microbial equilibrium, known as dysbiosis, contributes to the development and progression of various hepatic and pancreatic diseases. Through mechanisms such as increased intestinal permeability and exposure to microbial products-including lipopolysaccharide, trimethylamine-N-oxide, and secondary bile acids-dysbiosis promotes inflammation, oxidative stress, insulin resistance, and carcinogenesis. These changes are linked to conditions including metabolic dysfunction-associated steatotic liver disease, alcohol-associated liver disease, cirrhosis, hepatocellular carcinoma, pancreatitis, pancreatic ductal adenocarcinoma, and diabetes. Emerging tools like stool metagenomics and serum metabolomics help identify microbial biomarkers for diagnosis and risk stratification. While interventions such as probiotics, dietary changes, and fecal microbiota transplantation aim to restore microbial balance, their success remains inconsistent. This work aims to highlight the pathogenic role of GM across the GLPA, with special emphasis on the underexplored gut-pancreas connection. Advancing our understanding of the GLPA can unlock novel microbiota-targeted approaches for early diagnosis and treatment of hepatopancreatic diseases.
Core Tip: This editorial highlights the central role of gut microbiota in regulating the gut-liver-pancreas axis, a dynamic network critical for metabolic and immune homeostasis. Dysbiosis-driven disruptions-via microbial metabolites, barrier dysfunction, and immune imbalance-underlie the pathogenesis of liver and pancreatic diseases. While gut-liver interactions are well studied, gut-pancreas crosstalk remains underexplored. We emphasize emerging biomarkers, microbial-based therapies, and the urgent need for longitudinal studies and metabolomic profiling to translate microbiome science into precision diagnostics and treatments for hepatopancreatic disorders.
