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Abstract

Background

Metabolic dysfunction-associated steatohepatitis (MASH) is a progressive liver disorder that increases the risk of cirrhosis and liver-related death. Despite its growing prevalence, effective pharmacological treatments remain limited. Glucagon-like peptide-1 receptor agonists (GLP-1RAs) have emerged as potential agents capable of improving liver histology in patients with MASH.

Objective

This study aimed to evaluate the efficacy and safety of GLP-1 receptor agonists in promoting histological resolution of MASH and improving liver fibrosis in adults with biopsy-confirmed disease.

Methods

We systematically searched PubMed, Embase, Cochrane CENTRAL, and Scopus from inception to 27 June 2025 for randomized controlled trials comparing GLP-1 receptor agonists with placebo in adults with biopsy-proven MASH. The primary endpoint was MASH resolution without fibrosis progression; secondary endpoints were ≥1-stage fibrosis improvement and any adverse events. Study quality was assessed using the Cochrane Risk of Bias 2.0 tool. Pooled risk ratios (RRs) were estimated using a random-effects model.

Results

Three RCTs with a total of 1,172 participants were included. Treatment with GLP-1RAs significantly increased the likelihood of MASH resolution without fibrosis progression (RR = 2.04; 95% CI: 1.53–2.72; I² = 19%). GLP-1RAs also improved fibrosis without worsening of MASH (RR = 1.53; 95% CI: 1.24–1.89; I² = 0%). A modest rise in overall adverse events was observed (RR = 1.08; 95% CI: 1.02–1.14; I² = 9%), primarily reflecting mild to moderate gastrointestinal symptoms.

Conclusion

GLP-1 receptor agonists, particularly semaglutide and liraglutide, significantly enhance histologic outcomes in patients with biopsy-confirmed MASH while maintaining a favorable safety profile. These findings highlight the potential of GLP-1RAs as disease-modifying agents for MASH, especially in individuals with metabolic comorbidities.

Keywords

non-cirrhotic steatohepatitis incretin-based therapy histologic endpoint fatty liver disease liver biopsy trials insulin resistance cardiometabolic liver disease

Introduction

Metabolic dysfunction-associated steatohepatitis (MASH), formerly known as non-alcoholic steatohepatitis (NASH), represents a progressive hepatic condition characterized by fat accumulation in the liver, inflammatory cell infiltration, hepatocyte injury, and variable degrees of fibrosis.¹ It is a leading cause of cirrhosis, hepatocellular carcinoma, and liver transplantation, posing a growing global health concern, particularly among people with obesity and type 2 diabetes mellitus.^2,3 Despite increasing prevalence, pharmacological treatments for MASH remain scarce.³

Glucagon-like peptide-1 receptor agonists (GLP-1RAs) have attracted attention as potential therapeutic options due to their metabolic, anti-inflammatory, and hepatoprotective effects.⁴ Initially developed for glycaemic management in type 2 diabetes, these agents also contribute to weight loss, improved hepatic steatosis, and better insulin sensitivity.^5–7 Several recent randomized controlled trials (RCTs) have evaluated their impact on liver histology in individuals with biopsy-confirmed MASH.^8–10

Given the rising clinical interest in GLP-1RAs for MASH, a systematic summary of current findings is warranted. Accordingly, we performed a systematic review and meta-analysis of RCTs assessing the efficacy and safety of GLP-1RAs in adults with biopsy-confirmed MASH. The primary endpoint was histologic resolution of MASH without progression of fibrosis, while secondary endpoints included at least one-stage improvement in fibrosis and the incidence of adverse events. To our knowledge, this is the first meta-analysis restricted exclusively to randomized controlled trials in biopsy-confirmed MASH, using harmonized FDA-endorsed histologic endpoints. The purpose of this review is to consolidate available data to inform evidence-based clinical decisions and guideline development for the management of MASH. By focusing solely on high-quality biopsy trials, this review addresses a critical evidence gap and provides the most current and clinically interpretable synthesis of GLP-1RA effects on histologic outcomes in MASH.

Methods

Study design and registration

This review and meta-analysis adhered to the PRISMA 2020 guidelines.¹¹ Its aim was to assess the efficacy and safety of GLP-1RAs in patients with biopsy-confirmed MASH, emphasizing histological outcomes. The protocol, finalized prior to data extraction, outlined study selection, inclusion criteria, and analytical procedures, and was prospectively registered in the PROSPERO database (CRD420251135790).

Eligibility criteria

Eligible studies included randomized controlled trials enrolling adults with biopsy-confirmed MASH who received GLP-1RAs versus placebo. Trials were required to report at least one of the following outcomes: histological resolution of MASH without fibrosis worsening, improvement of fibrosis by at least one stage, or the occurrence of any adverse events. Resolution of MASH was defined by the absence of hepatocyte ballooning and minimal to no lobular inflammation, without any advancement in fibrosis stage.¹² Improvement in fibrosis was characterized as a reduction of at least one stage on the NASH Clinical Research Network (CRN) scale, provided that necroinflammatory activity did not worsen.¹³ Studies were excluded if they enrolled pediatric participants, lacked randomization, did not confirm MASH by biopsy, or failed to provide analyzable data.

Search strategy and study selection

A comprehensive search was performed across PubMed, Embase, Cochrane CENTRAL, and Scopus databases from inception to June 27, 2025. Both controlled vocabulary (e.g., MeSH terms such as “Glucagon-Like Peptide 1” and “Steatohepatitis”, and Emtree equivalents) and free-text keywords were used. Search terms were selected based on prior literature and indexing terminology for GLP-1 receptor agonists and MASH. Search strings combined terms such as “GLP-1 receptor agonist,” “semaglutide,” “liraglutide,” “nonalcoholic steatohepatitis,” “MASH,” “NASH,” “fibrosis,” “liver histology,” and “randomized trial.”

The pubmed search string was:

*(“Glucagon-Like Peptide 1”[MeSH] OR “GLP-1 receptor agonist” OR semaglutide OR liraglutide) AND (“Steatohepatitis”[MeSH] OR “nonalcoholic steatohepatitis” OR NASH OR MASH) AND (randomized OR placebo).

In Embase, the equivalent emtree-based string was:

(‘glucagon like peptide 1 receptor agonist”/exp OR ‘glp 1 receptor agonist’ OR semaglutide OR liraglutide) AND (‘steatohepatitis”/exp OR ‘nonalcoholic steatohepatitis’ OR NASH OR MASH) AND (random OR placebo).

Searches in central and scopus used the same key concepts:

(“GLP-1 receptor agonist” OR semaglutide OR liraglutide) AND (“nonalcoholic steatohepatitis” OR NASH OR MASH) AND (random OR placebo)**.

No language filters were applied. Additional studies were located by screening bibliographies of included trials and relevant reviews. After removing duplicates, two reviewers (CSK and AFZ) independently screened titles and abstracts, followed by full-text evaluations to confirm eligibility. Any disagreement was resolved through discussion or, when necessary, by consulting a third reviewer (SSH). The selection procedure was summarized in a PRISMA flowchart (Figure 1).

Figure 1.

PRISMA flow diagram for clinical trials.

Data extraction and outcome definitions

Two investigators (CSK and AFZ) independently retrieved data at both the study and outcome levels using a predesigned standardized extraction form. Extracted information included author details, publication year, country, sample size, study duration, intervention type, and dosage. Participant characteristics such as mean age, body mass index, and the proportion with type 2 diabetes were also recorded.

The primary endpoint was the proportion of participants achieving MASH resolution without fibrosis progression. The secondary endpoint involved at least a one-stage improvement in fibrosis without exacerbation of MASH activity. Safety outcomes included the frequency of any reported adverse events. When only percentages were provided, the event counts were derived based on sample size.

Risk of bias assessment

The quality of the included randomized trials was assessed using the Cochrane Risk of Bias 2.0 framework,¹⁴ which examines potential bias across five key domains: randomization process, deviations from intended interventions, incomplete data, outcome measurement, and selective reporting. Two authors (CSK and KT) conducted the assessments independently, resolving any discrepancies through consensus or, if required, by consultation with a third reviewer (SSH).

Each study was evaluated across five domains and assigned an overall risk rating of “low,” “some concerns,” or “high.”

A study was considered to have a low risk of bias only when all domains were rated as low.

If a study showed some concerns in one or more domains but none rated as high risk, it was classified as having some concerns overall.

Conversely, if one or more domains were rated as high risk, the study was deemed to have an overall high risk of bias.

All evaluations followed the Cochrane Handbook recommendations and were documented using the official Excel-based RoB 2.0 assessment template.

Statistical analysis

Data analysis was conducted using MetaXL version 5.3 (EpiGear International Pty Ltd, Sunrise Beach, Australia) as an Excel add-in. For binary outcomes, pooled risk ratios (RRs) with 95% confidence intervals (CIs) were estimated via the Mantel–Haenszel random-effects model to accommodate expected variability among studies.

Heterogeneity was evaluated using the I² statistic, where 25%, 50%, and 75% correspond to low, moderate, and high heterogeneity, respectively, representing the proportion of variation not attributable to chance. Cochran’s Q test was also applied to determine the statistical significance of heterogeneity, with p < 0.10 considered notable. Forest plots were produced within MetaXL to visualize pooled estimates.

Results

Study selection

The initial database search identified 312 articles. Following the removal of duplicates and screening of titles and abstracts, 14 studies underwent full-text review for eligibility. Ultimately, three randomized controlled trials (RCTs)^8–10 satisfied all inclusion criteria and were included in the quantitative synthesis.

Study characteristics

The three RCTs^8–10 collectively enrolled 1,172 adult participants, comprising 800 assigned to GLP-1 receptor agonist therapy and 372 receiving placebo (Table 1). All participants had biopsy-confirmed MASH, previously referred to as NASH, and histologic evaluation followed the NASH Clinical Research Network (CRN) criteria. The included RCTs were multinational^8,9 or conducted in the United Kingdom.¹⁰ All followed double-blind, placebo-controlled, randomized designs. Participants were primarily overweight or obese adults, with 33–62% having type 2 diabetes, and most presented with baseline fibrosis stages between F1 and F3. Treatment durations varied from 48 to 72 weeks. The mean participant age ranged from 50.0 to 56.3 years in the GLP-1RA arms and 52.0 to 55.4 years in the placebo groups. GLP-1RA regimens comprised semaglutide 0.1–0.4 mg daily or 2.4 mg once weekly, and liraglutide 1.8 mg daily, all delivered subcutaneously.

Table 1.

Study characteristics and main outcome data of included randomized controlled trials evaluating GLP-1 receptor agonists in adults with biopsy-proven MASH.

Study	Country	Study design	Population	Sample size (GLP-1RA vs placebo)	Mean age (years; GLP-1RA vs placebo)	Follow-up duration	GLP-1 regimen	MASH resolution (GLP-1RA vs placebo)	Fibrosis improvement (GLP-1RA vs placebo)	Any adverse events (GLP-1RA vs placebo)	Overall risk of bias
Newsome et al. (2020)	Multinational	Randomized, double-blind, placebo-controlled trial	Overweight/obese adults with MASH and F1–F3 fibrosis, 62% had type 2 diabetes	240 vs 80	55.2 (0.1 mg) vs 58.1 (0.2 mg) vs 54.3 (0.4 mg) vs 52.4 (placebo)	72 weeks	Semaglutide 0.1−0.4 mg SC OD	77/172 (44.8%) vs 10/58 (17.2%)	71/172 (41.3%) vs 19/58 (32.8%)	224/239 (93.7%) vs 67/80 (83.8%)	Low
Armstrong et al. (2016)	UK	Randomized, double-blind, placebo-controlled trial	Overweight/obese adults with MASH, 33% had type 2 diabetes	26 vs 26	50 vs 52	48 weeks	Liraglutide 1.8 mg SC OD	9/23 (39.1%) vs 2/22 (9.1%)	6/23 (26.1%) vs 3/22 (13.6%)	23/26 (88.5%) vs 24/26 (92.3%)	Low
Sanyal et al. (2025)	Multinational	Randomized, double-blind, placebo-controlled trial	Adults with MASH and F2–F3 fibrosis, 56% had type 2 diabetes	534 vs 266	56.3 vs 55.4	72 weeks	Semaglutide 2.4 mg SC once weekly	336/534 (62.9%) vs 91/266 (34.2%)	196/534 (36.7%) vs 60/266 (22.6%)	690/800 (86.3%) vs 315/395 (79.7%)	Low

According to the Cochrane RoB 2.0 tool, each study^8–10 demonstrated an overall low risk of bias.

Primary Outcome: Resolution of MASH Without Worsening of Fibrosis

All three RCTs^8–10 evaluated the proportion of participants achieving histological resolution of MASH without fibrosis progression. Resolution was consistently defined as the absence of ballooning and minimal or no lobular inflammation, with no increase in fibrosis stage.

In the pooled analysis, GLP-1RA therapy was associated with a markedly higher likelihood of achieving MASH resolution compared to placebo (RR = 2.04; 95% CI: 1.53–2.72). Heterogeneity across studies was low (I² = 19%; p = 0.29), supporting consistency of effect.

These findings indicate that GLP-1 receptor agonist treatment more than doubled the probability of histologic resolution of MASH without fibrosis progression compared with placebo (Figure 2).

Figure 2.

Forest plot of GLP-1 receptor agonists versus placebo for resolution of MASH without worsening of fibrosis.

Secondary Outcome: Improvement in Fibrosis Without Worsening of MASH

Each of the three RCTs^8–10 also investigated the proportion of participants showing at least a one-stage improvement in fibrosis without aggravation of MASH activity. This composite outcome captures both fibrosis regression and stabilization or resolution of necroinflammatory features.

The meta-analysis demonstrated a significant advantage for GLP-1RAs, with a pooled RR of 1.53 (95% CI: 1.24–1.89) and no heterogeneity (I² = 0%). This consistent effect across studies suggests an antifibrotic benefit, albeit of smaller magnitude than that observed for MASH resolution (Figure 3).

Figure 3.

Forest plot of GLP-1 receptor agonists versus placebo for improvement in fibrosis (≥1 stage) without worsening of MASH.

Safety Outcomes: Any Adverse Events

All included RCTs^8–10 provided safety data. The pooled estimate revealed a slight but statistically significant increase in overall adverse events among participants receiving GLP-1RAs, largely attributed to gastrointestinal symptoms such as nausea, vomiting, and diarrhea. The pooled RR was 1.08 (95% CI: 1.02–1.14; p = 0.33; I² = 9%), indicating minimal between-study variability (Figure 4).

Figure 4.

Forest plot comparing the incidence of any adverse event between GLP-1 receptor agonists and placebo.

These adverse effects were predominantly mild to moderate in intensity and infrequently resulted in treatment discontinuation.

Discussion

This systematic review and meta-analysis integrates current randomized trial evidence assessing the efficacy and safety of GLP-1 receptor agonists (GLP-1RAs) in adults with biopsy-confirmed MASH. The collective findings strengthen the case for semaglutide and liraglutide as promising therapeutic agents that address both metabolic and histologic aspects of MASH while preserving a favorable safety profile.

Achieving MASH resolution without fibrosis progression is recognized as a principal endpoint in contemporary clinical research, as it correlates strongly with long-term improvements in liver outcomes—such as lower risks of cirrhosis progression and hepatocellular carcinoma.^15,16 In this analysis, GLP-1RA treatment was associated with substantially higher rates of MASH resolution compared with placebo. This improvement likely arises from the broad metabolic actions of GLP-1RAs, including significant weight loss, amelioration of insulin resistance, decreased hepatic steatosis, and suppression of pro-inflammatory signaling.^4–7

Notably, these histologic benefits occurred without a corresponding rise in fibrosis severity, supporting the hypothesis that GLP-1RAs mitigate hepatocellular injury and inflammation—the defining features of active MASH—without inducing fibrotic remodeling.¹⁷ This property distinguishes GLP-1RAs from several other investigational therapies that may reduce steatosis or inflammation but lack consistent effects on fibrosis.

While MASH resolution represents an essential therapeutic goal, fibrosis stage remains the strongest determinant of long-term outcomes, including liver-related mortality and morbidity.^18,19 In our pooled findings, improvement in fibrosis was more frequent among GLP-1RA recipients, though absolute rates of ≥1-stage regression remained modest. This modest change is unsurprising given the relatively short treatment durations (48–72 weeks) and the typically gradual pace of fibrosis recovery. Nevertheless, the direction of effect suggests that GLP-1RAs may facilitate not only histologic remission but also structural hepatic improvement.

The observed regression of fibrosis is likely an indirect effect, arising from reduced hepatic inflammation and correction of underlying metabolic dysfunction, rather than a direct antifibrotic mechanism.^20–22 Even so, small improvements in fibrosis confer prognostic advantages,¹⁶ and the reproducibility of this effect across studies enhances the robustness of the evidence.

Safety remains a key consideration for therapies intended for chronic use in largely asymptomatic patients. Across the analyzed RCTs, adverse events occurred frequently in both GLP-1RA and placebo arms, consistent with rigorous trial monitoring. However, the vast majority of adverse effects were mild to moderate—predominantly gastrointestinal—and aligned with the established tolerability profile of GLP-1RAs in metabolic indications. Gastrointestinal side effects, including nausea, vomiting, and diarrhea, were the most frequently reported adverse events, consistent with the established safety profile of GLP-1RAs. Although the incidence of these events was slightly higher in the active treatment arms of two trials,^8,9 they were generally mild to moderate in severity and seldom resulted in treatment discontinuation.

The occurrence of serious adverse events was low and comparable between GLP-1RA and placebo groups, reaffirming their acceptable safety margin in this population. Importantly, no novel safety signals were identified beyond those already recognized in trials of GLP-1RAs for diabetes and obesity management.

These findings highlight the potential of GLP-1RAs to serve as dual-benefit agents for individuals with MASH who also have metabolic comorbidities such as type 2 diabetes or obesity. In addition to their direct hepatic effects, GLP-1RAs improve several extrahepatic metabolic pathways—including weight regulation, insulin sensitivity, and cardiometabolic risk factors—that are closely intertwined with MASH pathophysiology. These systemic benefits may therefore contribute to, and help sustain, favourable liver outcomes. Their established ability to reduce cardiovascular risk and promote meaningful weight loss²³ further supports their role as a comprehensive therapeutic option for patients with multisystem metabolic disease. Accordingly, major clinical guidelines—such as those issued by the AASLD²⁴ and EASL²⁵—have begun to recognize GLP-1RAs as viable options for MASH management, particularly in individuals with overlapping metabolic syndrome.

Nonetheless, several limitations should be acknowledged. The number of eligible RCTs remains modest, with variable sample sizes and treatment durations. Differences in trial inclusion criteria and GLP-1RA dosing regimens may also influence generalizability. Moreover, the histologic endpoints used in these trials, although informative, are surrogate measures that may not fully reflect long-term clinical outcomes, such as cirrhosis, hepatic decompensation, or mortality.

Future investigations should emphasize extended follow-up to determine the durability of histologic improvements, fibrosis regression, and downstream clinical events such as progression to cirrhosis or the need for liver transplantation. Comparative trials involving other emerging pharmacologic agents—such as resmetirom or lanifibranor—will be crucial to delineate the optimal therapeutic positioning of GLP-1RAs within the evolving treatment landscape for MASH.

Conclusion

This systematic review and meta-analysis suggests that GLP-1 receptor agonists, including semaglutide and liraglutide, may offer histologic benefits in adults with biopsy-confirmed MASH. Although the number of trials and total sample size were limited, GLP-1RAs were consistently associated with higher rates of MASH resolution without worsening of fibrosis, and they showed a possible, though less certain, effect on fibrosis improvement.

Although adverse events occur more frequently with GLP-1RAs, they are typically mild to moderate and align with the well-recognized gastrointestinal tolerability profile of this therapeutic class.

Given their combined metabolic and hepatic benefits, GLP-1 receptor agonists emerge as promising candidates for the management of MASH, particularly among individuals who also have obesity or type 2 diabetes. The current evidence reinforces their growing role in liver-targeted therapy and highlights their potential as disease-modifying treatments for MASH. Nevertheless, larger and longer-duration randomized trials are essential to verify their effects on fibrosis regression and on clinically meaningful endpoints such as cirrhosis, hepatic decompensation, and liver-related mortality.

Footnotes

ORCID iDs

Kaeshaelya Thiruchelvam

Abdullah Faiz Zaihan

Author contributions

CSK: Conceptualization; Methodology; Formal analysis; Writing – original draft; Writing – review & editing.

KT: Data curation; Methodology; Writing – original draft; Visualization.

SSH: Supervision; Validation; Writing – review & editing.

AFZ: Data curation; Formal analysis; Writing – review & editing; Project administration. All authors have read and approved the final manuscript.

Funding

The authors received no financial support for the research, authorship, and/or publication of this article.

Declaration of conflicting interests

The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Data Availability Statement

Data sharing is not applicable to this article as no datasets were generated or analysed during the current study.*

Authorship statement

All authors meet the ICMJE authorship criteria.

References

Sandireddy

Sakthivel

Gupta

, et al. Systemic impacts of metabolic dysfunction-associated steatotic liver disease (MASLD) and metabolic dysfunction-associated steatohepatitis (MASH) on heart, muscle, and kidney related diseases. Front Cell Dev Biol 2024; 12: 1433857.

Kabarra

Golabi

Younossi

. Nonalcoholic steatohepatitis: global impact and clinical consequences. Endocr Connect 2021; 10(10): R240–R247.

Kakde

Mushtaq

Liaqat

, et al. Emerging therapies for Non-Alcoholic Steatohepatitis (NASH): a comprehensive review of pharmacological and non-pharmacological approaches. Cureus 2024; 16(9): e69129.

Ghazanfar

Kandhi

Nawaz

, et al. Role of glucagon-like peptide-1 receptor agonists in the management of non-alcoholic steatohepatitis: a clinical review article. Cureus 2021; 13(5): e15141.

Bołdys

Bułdak

Nicze

, et al. Liraglutide reduces liver steatosis and improves metabolic indices in obese patients without diabetes: a 3-month prospective study. Int J Mol Sci 2025; 26(12): 5883.

Zhu

Zhang

, et al. Efficacy and safety of GLP-1 receptor agonists in patients with type 2 diabetes mellitus and non-alcoholic fatty liver disease: a systematic review and meta-analysis. Front Endocrinol 2021; 12: 769069.

Guo

Tian

Lin

, et al. Liraglutide or insulin glargine treatments improves hepatic fat in obese patients with type 2 diabetes and nonalcoholic fatty liver disease in twenty-six weeks: a randomized placebo-controlled trial. Diabetes Res Clin Pract 2020; 170: 108487.

Sanyal

Newsome

Kliers

, et al. Phase 3 trial of semaglutide in metabolic dysfunction-associated steatohepatitis. N Engl J Med 2025; 392(21): 2089–2099.

Newsome

Buchholtz

Cusi

, et al. A placebo-controlled trial of subcutaneous semaglutide in nonalcoholic steatohepatitis. N Engl J Med 2021; 384(12): 1113–1124.

10.

Armstrong

Gaunt

Aithal

, et al. Liraglutide safety and efficacy in patients with non-alcoholic steatohepatitis (LEAN): a multicentre, double-blind, randomised, placebo-controlled phase 2 study. Lancet 2016; 387(10019): 679–690.

11.

Page

McKenzie

Bossuyt

, et al. The PRISMA 2020 statement: an updated guideline for reporting systematic reviews. BMJ 2021; 372: n71.

12.

Cheung

Neuschwander-Tetri

Kleiner

, et al. Defining improvement in nonalcoholic steatohepatitis for treatment trial endpoints: recommendations from the liver forum. Hepatology 2019; 70(5): 1841–1855.

13.

Harvey

. NASH: regulatory considerations for clinical drug development and U.S. FDA approval. Acta Pharmacol Sin 2022; 43(5): 1210–1214.

14.

Sterne

JAC

Savović

Page

, et al. RoB 2: a revised tool for assessing risk of bias in randomised trials. BMJ 2019; 366: l4898.

15.

Wang

Xiao

, et al. A review of MASLD-Related hepatocellular carcinoma: progress in pathogenesis, early detection, and therapeutic interventions. Front Med (Lausanne) 2024; 11: 1410668.

16.

Sanyal

Anstee

Trauner

, et al. Cirrhosis regression is associated with improved clinical outcomes in patients with nonalcoholic steatohepatitis. Hepatology 2022; 75(5): 1235–1246.

17.

Fang

Zeng

, et al. Effects of GLP-1 receptor agonists on the degree of liver fibrosis and CRP in non-alcoholic fatty liver disease and non-alcoholic steatohepatitis: a systematic review and meta-analysis. Prim Care Diabetes 2024; 18(3): 268–276.

18.

Lim

Hui Lim

, et al. Mortality outcomes by fibrosis stage in nonalcoholic fatty liver disease: a systematic review and meta-analysis. Clin Gastroenterol Hepatol 2023; 21(4): 931–939.e5.

19.

Sanyal

Van Natta

Clark

, et al. Prospective study of outcomes in adults with nonalcoholic fatty liver disease. N Engl J Med 2021; 385(17): 1559–1569.

20.

Tsiampali

Vachliotis

Goulas

, et al. Animal studies on glucagon-like peptide-1 receptor agonists and related polyagonists in nonalcoholic fatty liver disease. Hormones (Athens) 2024; 23(4): 611–619.

21.

Yabut

Drucker

. Glucagon-like Peptide-1 receptor-based therapeutics for metabolic liver disease. Endocr Rev 2023; 44(1): 14–32.

22.

Zeng

Huang

Zhu

, et al. Mechanism-guided drug development and treatment for liver fibrosis: a clinical perspective. Front Pharmacol 2025; 16: 1574385.

23.

Lincoff

Brown-Frandsen

Colhoun

, et al. Semaglutide and cardiovascular outcomes in obesity without diabetes. N Engl J Med 2023; 389(24): 2221–2232.

24.

Rinella

Neuschwander-Tetri

Siddiqui

, et al. AASLD practice guidance on the clinical assessment and management of nonalcoholic fatty liver disease. Hepatology 2023; 77(5): 1797–1835.

25.

European Association for the Study of the Liver (EASL); European Association for the Study of Diabetes (EASD); European Association for the Study of Obesity (EASO) . EASL-EASD-EASO clinical practice guidelines on the management of Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD). J Hepatol 2024; 81(3): 492–542.

Efficacy and safety of GLP-1 receptor agonists in metabolic dysfunction-associated steatohepatitis: A systematic review and meta-analysis of randomized controlled trials

Abstract

Background

Objective

Methods

Results

Conclusion

Keywords

Introduction

Methods

Study design and registration

Eligibility criteria

Search strategy and study selection

Data extraction and outcome definitions

Risk of bias assessment

Statistical analysis

Results

Study selection

Study characteristics

Primary Outcome: Resolution of MASH Without Worsening of Fibrosis

Secondary Outcome: Improvement in Fibrosis Without Worsening of MASH

Safety Outcomes: Any Adverse Events

Discussion

Conclusion

Footnotes

ORCID iDs

Author contributions

Funding

Declaration of conflicting interests

Data Availability Statement

Authorship statement

References