Pandey H, Goel P, Srinivasan VM, Tang DWT, Wong SH, Lal D. Gut microbiota in non-alcoholic fatty liver disease: Pathophysiology, diagnosis, and therapeutics. World J Hepatol 2025; 17(6): 106849 [DOI: 10.4254/wjh.v17.i6.106849]
Corresponding Author of This Article
Devi Lal, Assistant Professor, Department of Zoology, Ramjas College, University of Delhi, University Road, University Enclave, Delhi 110007, India. devilal@ramjas.du.ac.in
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Review
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. Jun 27, 2025; 17(6): 106849 Published online Jun 27, 2025. doi: 10.4254/wjh.v17.i6.106849
Gut microbiota in non-alcoholic fatty liver disease: Pathophysiology, diagnosis, and therapeutics
Himani Pandey, Prabudh Goel, Varunvenkat M Srinivasan, Daryl W T Tang, Sunny H Wong, Devi Lal
Himani Pandey, Department of Medical Genetics, Redcliffe Labs, Noida 201301, Uttar Pradesh, India
Prabudh Goel, Department of Pediatric Surgery, All India Institute of Medical Sciences, Delhi 110029, India
Varunvenkat M Srinivasan, Department of Medical Genetics, Postgraduate Institute of Child Health, Noida 201310, Uttar Pradesh, India
Daryl W T Tang, Sunny H Wong, Lee Kong Chian School of Medicine, Nanyang Technological University, Singapore 308232, Singapore
Devi Lal, Department of Zoology, Ramjas College, University of Delhi, Delhi 110007, India
Co-first authors: Himani Pandey and Prabudh Goel.
Co-corresponding authors: Sunny H Wong and Devi Lal.
Author contributions: Pandey H and Goel P contributed equally to this article and as co-first authors of this manuscript. Pandey H, Goel P, Wong SH, and Lal D conceptualized and designed the study; Pandey H, Goel P, Srinivasan VM, Tang DWT, Wong SH, and Lal D carried out literature search; Tang DWT prepared the diagrams; Pandey H, Goel P, Wong SH, and Lal D prepared the original draft; Pandey H, Goel P, Srinivasan VM, Tang DWT, Wong SH, and Lal D reviewed and edited the manuscript; Wong SH and Lal D carried out the supervision and they contributed equally to this manuscript and as co-corresponding authors of this manuscript; and all authors read and agreed to the published version of the manuscript.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
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: Devi Lal, Assistant Professor, Department of Zoology, Ramjas College, University of Delhi, University Road, University Enclave, Delhi 110007, India. devilal@ramjas.du.ac.in
Received: March 9, 2025 Revised: March 25, 2025 Accepted: May 21, 2025 Published online: June 27, 2025 Processing time: 108 Days and 22.9 Hours
Abstract
Non-alcoholic fatty liver disease (NAFLD), also referred to as metabolic-associated fatty liver disease, is among the most prevalent chronic liver conditions. In some cases, NAFLD may lead to liver inflammation and non-alcoholic steatohepatitis, which can eventually progress to liver cirrhosis and hepatocellular carcinoma. The pathophysiology of NAFLD is complex, involving both genetic and environmental factors. NAFLD is a multisystem disease linked to a higher likelihood of developing metabolic disorders such as type 2 diabetes, obesity, and cardiovascular and chronic kidney diseases. The gut-liver axis represents a key connection between the gut microbiota and the liver, and its disruption has been linked to NAFLD. Growing evidence underscores the significant role of gut microbiota in the onset and progression of NAFLD, with alterations in the gut microbiome and impaired gut barrier function. Studies have identified key microbiota signatures and metabolites linked to NAFLD, implicating oxidative stress, endotoxemia, and inflammatory pathways that further strengthen the connection between gut microbiota and NAFLD. Modulation of gut microbiota through diet and microbiota-centered therapies, such as next-generation probiotics and fecal microbiota transplantation, holds promise for treating NAFLD. In this review, we explore the key link between gut microbiota and the development and progression of NAFLD, as well as its potential applications in the diagnosis and treatment of the disease.
Core Tip: Non-alcoholic fatty liver disease (NAFLD) is among the most prevalent chronic liver conditions that has been recognized as an emerging global health problem. Evidence suggests that the gut microbiota plays a critical role in the pathophysiology of NAFLD by influencing liver inflammation through its metabolites. Identifying gut microbial and metabolic signatures opens new avenues for early diagnosis and therapeutic interventions. Microbiota-targeted therapies, including diet, probiotics, prebiotics, synbiotics, and fecal microbiota transplantation, hold promise for alleviating NAFLD and improving patient outcomes.
