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S2817 Do All Weight-Loss Drugs Benefit the Liver? Real-World FibroScan Outcomes Across FDA-Approved Anti-Obesity Pharmacotherapies in MASLD
Abstract   Peer reviewed

S2817 Do All Weight-Loss Drugs Benefit the Liver? Real-World FibroScan Outcomes Across FDA-Approved Anti-Obesity Pharmacotherapies in MASLD

Nikhil Vasireddi, Anika Mittal, Jackson Snyder, Christopher Jun, Patrick Ten Eyck, Linder Wendt, Mohamad Mokadem and Antonio Sanchez
The American journal of gastroenterology, Vol.121(10S1), pp.S612-S612
10/01/2026
DOI: 10.14309/01.ajg.0001220520.44811.7b

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Abstract

Introduction: Metabolic dysfunction-associated steatotic liver disease (MASLD) affects >30% of adults globally. To our knowledge, this study presents the first comparison of hepatic outcomes across various United States Food and Drug Administration (FDA)-approved weight-loss pharmacotherapies. Methods: Retrospective, single-center analysis (January 2015–October 2025) was performed of patients from a weight management clinic who received at least 1 FDA-approved weight-loss medication (liraglutide, semaglutide, tirzepatide, phentermine, phentermine/topiramate, or bupropion/naltrexone), and underwent serial VCTE (FibroScan). Per American Association for the Study of Liver Diseases guidelines, MASLD was defined as baseline CAP ≥275 dB/m with ≥1 cardiometabolic risk factor and no history of alcohol use disorder. Patients were classified as glucagon-like peptide-1 receptor agonist (GLP-1 RA) only, combination GLP-1 RA + non-GLP-1, or non-GLP-1 only. Primary outcomes were ΔCAP (dB/m) and ΔLiver Stiffness (ΔLS, kPa). Intragroup changes were assessed by Wilcoxon signed-rank test; intergroup by Kruskal-Wallis + Bonferroni-corrected Dunn post-hoc (α = 0.05). Multivariable linear regression adjusted for age, sex, comorbid metabolic burden, follow-up time, and baseline CAP and LS (Model 1), with a second model adding percent weight change (Model 2). Results: Among 219 patients meeting MASLD criteria, all groups achieved significant intragroup CAP reductions: GLP-1 only (−46.5 ± 83.8 dB/m, P = 0.007), Combination (−54.4 ± 86.4, P < 0.001), and Non-GLP-1 (−30.1 ± 57.8, P = 0.002). Significant LS reductions were observed in GLP-1 (−1.8 ± 8.7 kPa, P = 0.048) and Combination (−1.9 ± 13.5 kPa, P = 0.003) groups, but not Non-GLP-1 (P = 0.376). Intergroup differences were not significant (ΔCAP P = 0.418; ΔLS P = 0.102). On multivariable regression, combination therapy was independently associated with greater LS improvement than non-GLP-1 (Model 1: β = 4.40 [0.47–8.33], P = 0.029; Model 2 +%WT: β = 5.20 [0.99–9.41], P = 0.016), with increasing coefficient magnitude after weight adjustment suggesting a potential weight-independent GLP-1 hepatic effect. FIB-4 and NFS did not significantly change in any group. Conclusion: In this real-world weight management cohort, GLP-1-containing regimens achieved significant reductions in hepatic steatosis and liver stiffness. Combination GLP-1 RA therapy was independently associated with LS improvement even after weight adjustment, supporting a direct hepatic GLP-1 effect. FIB-4 and NFS may not be effective fibrosis screening and monitoring tools. Prospective, histology-based studies are needed.
 Metabolism Drug therapy FDA approval GLP-1 receptor agonists Liver

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