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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. Oct 27, 2026; 18(10): 125275
Published online Oct 27, 2026. doi: 10.4254/wjh.125275
Incretin-based therapies in hepatology practice
Merve Eren Durmus, Gokhan Koker, Serkan Ocal
Merve Eren Durmus, Serkan Ocal, Department of Gastroenterology, University of Health Sciences, Antalya Training and Research Hospital, Antalya 07100, Türkiye
Gokhan Koker, Department of Internal Medicine, University of Health Sciences, Antalya Training and Research Hospital, Antalya 07100, Türkiye
Author contributions: Durmus ME and Koker G conceptualized and designed the review, performed the literature review and drafted the manuscript; Koker G and Ocal S critically revised the manuscript for important intellectual content; all authors approved the final version of the manuscript and agree to be accountable for all aspects of the work.
AI contribution statement: No artificial intelligence (AI) tools were used in the research, analysis, interpretation, writing, or editing of this manuscript. The authors take full responsibility for the integrity, accuracy, originality, and scientific validity of the manuscript and all submitted materials.
Conflict-of-interest statement: The authors declare that they have no conflict of interest.
Corresponding author: Gokhan Koker, MD, Associate Professor, Department of Internal Medicine, University of Health Sciences, Antalya Training and Research Hospital, Varlik St. Antalya Training and Research Hospital, Antalya 07100, Türkiye. gokhan.koker@sbu.edu.tr
Received: July 7, 2026
Revised: July 31, 2026
Accepted: August 31, 2026
Published online: October 27, 2026
Processing time: 111 Days and 5.6 Hours
Abstract

Glucagon-like peptide-1 receptor agonists and dual incretin therapies are now encountered routinely in hepatology, well beyond their initial use as glucose-lowering agents. Their relevance to steatotic liver disease is largely indirect. By reducing obesity, insulin resistance, adipose tissue dysfunction, systemic inflammation and cardiometabolic risk, they address several processes underpinning metabolic dysfunction-associated steatotic liver disease and, in some patients, metabolic dysfunction-associated steatohepatitis. Biopsy-based trials have shown improvement in steatohepatitis activity, while recent studies of semaglutide, tirzepatide and glucagon-like peptide-1/glucagon co-agonists have also reported favorable fibrosis-related findings. Real-world cohorts suggest lower rates of progression to cirrhosis, decompensation and hepatocellular carcinoma, although the results are inconsistent and remain open to residual confounding. These observations should be interpreted carefully in clinical practice. Loss of body weight or decreased aminotransferase levels should not be treated as proof of hepatic benefit, nor should incretin therapy be regarded as liver-directed treatment on those grounds alone. A more appropriate approach is to place these agents within a fibrosis-based pathway that includes baseline risk assessment, sequential non-invasive testing, attention to nutritional status and frailty, and continued cirrhosis and hepatocellular carcinoma surveillance in patients with established advanced liver disease. This review examines the available evidence and outlines a practical algorithm for hepatology care.

Keywords: Glucagon-like peptide-1 receptor agonists; Tirzepatide; Dual incretin therapy; Metabolic dysfunction-associated steatotic liver disease; Metabolic dysfunction-associated steatohepatitis; Steatotic liver disease; Liver fibrosis; Hepatocellular carcinoma; Frailty; Resmetirom

Core Tip: Incretin-based therapies are important in hepatology because they act on the metabolic drivers of steatotic liver disease. Their hepatic benefit should be judged by fibrosis-oriented monitoring rather than by weight loss. Histological and real-world data are encouraging, but whether these drugs prevent decompensation, hepatocellular carcinoma, transplantation or liver-related death is unclear. They are best regarded as partners to liver-directed therapy, not as replacements for standard cirrhosis care and surveillance.

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