A Placebo-controlled trial of subcutaneous semaglutide in nonalcoholic steatohepatitis
Open accessAbstract
BACKGROUND: Nonalcoholic steatohepatitis (NASH) is a common disease that is associated with increased morbidity and mortality, but treatment options are limited. The efficacy and safety of the glucagon-like peptide-1 receptor agonist semaglutide in patients with NASH is not known. METHODS: We conducted a 72-week, double-blind phase 2 trial involving patients with biopsy-confirmed NASH and liver fibrosis of stage F1, F2, or F3. Patients were randomly assigned, in a 3:3:3:1:1:1 ratio, to receive once-daily subcutaneous semaglutide at a dose of 0.1, 0.2, or 0.4 mg or corresponding placebo. The primary end point was resolution of NASH with no worsening of fibrosis. The confirmatory secondary end point was an improvement of at least one fibrosis stage with no worsening of NASH. The analyses of these end points were performed only in patients with stage F2 or F3 fibrosis; other analyses were performed in all the patients. RESULTS: In total, 320 patients (of whom 230 had stage F2 or F3 fibrosis) were randomly assigned to receive semaglutide at a dose of 0.1 mg (80 patients), 0.2 mg (78 patients), or 0.4 mg (82 patients) or to receive placebo (80 patients). The percentage of patients in whom NASH resolution was achieved with no worsening of fibrosis was 40% in the 0.1-mg group, 36% in the 0.2-mg group, 59% in the 0.4-mg group, and 17% in the placebo group (P<0.001 for semaglutide 0.4 mg vs. placebo). An improvement in fibrosis stage occurred in 43% of the patients in the 0.4-mg group and in 33% of the patients in the placebo group (P = 0.48). The mean percent weight loss was 13% in the 0.4-mg group and 1% in the placebo group. The incidence of nausea, constipation, and vomiting was higher in the 0.4-mg group than in the placebo group (nausea, 42% vs. 11%; constipation, 22% vs. 12%; and vomiting, 15% vs. 2%). Malignant neoplasms were reported in 3 patients who received semaglutide (1%) and in no patients who received placebo. Overall, neoplasms (benign, malignant, or unspecified) were reported in 15% of the patients in the semaglutide groups and in 8% in the placebo group; no pattern of occurrence in specific organs was observed. CONCLUSIONS: This phase 2 trial involving patients with NASH showed that treatment with semaglutide resulted in a significantly higher percentage of patients with NASH resolution than placebo. However, the trial did not show a significant between-group difference in the percentage of patients with an improvement in fibrosis stage. (Funded by Novo Nordisk; ClinicalTrials.gov number, NCT02970942.).
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GLP-1 RAs are indicated for the treatment of type 2 diabetes (all) and obesity (liraglutide and semaglutide only) and have beneficial effects on patient-important outcomes such as weight loss, cardiovascular and kidney events, hepatic steatosis, and mortality.
“Clinically, GLP-1 RAs are indicated for the treatment of type 2 diabetes (all) and obesity (liraglutide and semaglutide only) and have beneficial effects on patient-important outcomes such as weight loss, cardiovascular and kidney events, hepatic steatosis, and mortality.5,7–9,11,30”
From Glucagon-Like Peptide-1 Receptor Agonists and Thyroid Cancer: A Narrative Review (2024) · cites this paper as [30]
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredIn studies of liraglutide, semaglutide, and tirzepatide for MASLD, the primary outcome was resolution of fatty liver disease without worsening of fibrosis, and significant improvements were noted.
“The primary outcome for all three studies was resolution of fatty liver disease without worsening of fibrosis, and significant improvements were noted.”
From GLP-1 receptor agonists and next-generation incretin-based medications: metabolic, cardiovascular, and renal benefits (2026) · cites this paper as [82]
The Efficacy section (p. 5) identifies NASH resolution without worsening of fibrosis as this semaglutide trial’s primary end point and reports a significant improvement versus placebo. This paper does not establish that the liraglutide and tirzepatide studies had the same primary outcome or significant results. Its Results (p. 2) also distinguish the significant NASH-resolution result from the nonsignificant improvement in fibrosis stage. (LLM, conf=0.87)
Experimental — accuracy not yet measuredA 2020 clinical trial involving patients with nonalcoholic steatohepatitis revealed a 15% incidence of tumors (benign, malignant, or unspecified) (35/239) among those administered semaglutide, compared to 8% (6/80) in the control group.
“Notably, a 2020 clinical trial involving patients with nonalcoholic steatohepatitis (NASH) revealed a 15% incidence of tumors (benign, malignant, or unspecified) (35/239) among those administered semaglutide, compared to 8% (6/80) in the control group [108].”
From Exploring the Side Effects of GLP-1 Receptor Agonist: To Ensure Its Optimal Positioning (2025) · cites this paper as [108]
The Safety section (p. 8) reports 35 neoplasms across the semaglutide groups (15%) and 6 in the placebo group (8%); the adverse-events table (p. 10) gives denominators of 239 and 80, respectively. The year is inaccurate: the publication is dated 2021 (p. 1), and the Patients section (p. 5) says enrollment occurred in 2017–2018, not 2020. (LLM, conf=0.88)
Experimental — accuracy not yet measuredIn the same 72-week phase 2 RCT, fibrosis improvement with semaglutide (43% vs 33%) did not reach significance.
“Fibrosis improvement (43% vs. 33%) did not reach significance, likely due to study duration.”
From Precision obesity medicine: A phenotype-guided framework for pharmacologic therapy across the lifespan (2025) · cites this paper as [54]
The Efficacy section (p. 5) reports fibrosis improvement in 43% of the semaglutide 0.4-mg group versus 33% of the placebo group after 72 weeks, a nonsignificant difference (P=0.48). The Discussion (p. 11) says insufficient study duration was possible, but also identifies inadequate statistical power as a possible explanation; it does not establish duration as the likely cause. (LLM, conf=0.86)
Experimental — accuracy not yet measuredIn a 72-week phase 2 RCT of 1197 participants with biopsy-confirmed MASH and F2-F3 fibrosis, semaglutide 0.4 mg/day achieved significant MASH resolution in 59% vs 17% with placebo.
“In a 72-week phase 2 RCT of 1197 participants with biopsy-confirmed MASH and F2–F3 fibrosis, semaglutide 0.4 mg/day achieved a significant MASH resolution in 59% vs. 17% with placebo [54].”
From Precision obesity medicine: A phenotype-guided framework for pharmacologic therapy across the lifespan (2025) · cites this paper as [54]
The Efficacy section (p. 5) reports significantly greater NASH resolution without worsening of fibrosis at 72 weeks with semaglutide 0.4 mg daily than with placebo (59% vs. 17%) among patients with F2–F3 fibrosis. However, the Results (p. 2) report 320 randomized participants, not 1197, and the Methods (p. 2) state that the trial also enrolled patients with F1 fibrosis; the F2–F3 restriction applied to the primary-endpoint analysis. (LLM, conf=0.90)
Experimental — accuracy not yet measured
In MASLD and MASH, semaglutide induces histological improvement, including MASH resolution and fibrosis regression, with >60% of patients achieving resolution in F2-F3 stages.
“In MASLD and MASH, semaglutide induces histological improvement, including MASH resolution and fibrosis regression, with > 60% of patients achieving resolution in F2–F3 stages.”
From Precision obesity medicine: A phenotype-guided framework for pharmacologic therapy across the lifespan (2025) · cites this paper as [54]
The Efficacy section (p. 5) reports significantly greater NASH resolution with 0.4-mg semaglutide in patients with F2–F3 fibrosis, but the primary analysis found 59%, not more than 60%; a sensitivity analysis found 62%. The Discussion (p. 9) reports no significant between-group difference in fibrosis-stage improvement, so the claim of fibrosis regression overstates the finding. (LLM, conf=0.92)
Experimental — accuracy not yet measuredLiraglutide and semaglutide treatments were accompanied by HbA1c reduction of 0.5% and 1.2%, respectively.
“Both treatments were accompanied by a weight loss of 5.5 % and 12.5 % as well as a HbA1c reduction of 0.5 % and 1.2 %, respectively.”
From Obesity and MASLD: Is weight loss the (only) key to treat metabolic liver disease? (2024) · cites this paper as [109]
The Efficacy section (p. 7) reports dose-dependent reductions in glycated hemoglobin with semaglutide. It does not give a 1.2% reduction in the retrieved passage, and this trial did not test liraglutide or report a 0.5% reduction for it (Procedures, p. 3). (LLM, conf=0.85)
Experimental — accuracy not yet measuredLiraglutide and semaglutide treatments were accompanied by weight loss of 5.5% and 12.5%, respectively.
“Both treatments were accompanied by a weight loss of 5.5 % and 12.5 % as well as a HbA1c reduction of 0.5 % and 1.2 %, respectively.”
From Obesity and MASLD: Is weight loss the (only) key to treat metabolic liver disease? (2024) · cites this paper as [109]
The Efficacy section (p. 7) reports weight loss with semaglutide, including a mean of 13% at the 0.4-mg dose, rather than the stated 12.5%. The paper did not test liraglutide, and its discussion of that drug does not report the claimed 5.5% weight loss. (LLM, conf=0.87)
Experimental — accuracy not yet measuredThe largest available trial on semaglutide in MASH (vs. placebo over an 18-month treatment period) demonstrated resolution of steatohepatitis but no fibrosis improvement.
“The largest available trial on semaglutide in MASH ( vs . placebo over an 18-month treatment period) demonstrated resolution of steatohepatitis but no fi brosis improvement.”
From EASL-EASD-EASO Clinical Practice Guidelines on the management of metabolic dysfunction-associated steatotic liver disease (MASLD). (2024) · cites this paper as [401]
The Efficacy results (p. 5) show significantly more NASH resolution with semaglutide than placebo, but no statistically significant difference in fibrosis-stage improvement—not an absence of improvement. Trial Design and Oversight (p. 3) specifies a 72-week treatment period, rather than 18 months. Our copy also does not establish that this was the largest available trial. (LLM, conf=0.88)
Experimental — accuracy not yet measuredAccruing randomized clinical trial data suggest that pioglitazone, GLP-1 RA, and a dual GIP and GLP-1 RA have potential benefits in terms of decreasing hepatic steatosis and in the resolution of MASH without worsening of fibrosis in individuals with biopsy-proven MASH or those at higher risk of clinically significant liver fibrosis identified with noninvasive tests.
“Accruing randomized clinical trial data suggest that pioglitazone, GLP-1 RA, and a dual GIP and GLP-1 RA have potential benefits in terms of decreasing hepatic steatosis and in the resolution of MASH without worsening of fibrosis in individuals with biopsy-proven MASH or those at higher risk of clinically significant liver fibrosis identified with noninvasive tests (146-153).”
From 9. Pharmacologic Approaches to Glycemic Treatment: Standards of Care in Diabetes—2025 (2025) · cites this paper as [150]
The Efficacy section (p. 5) reports that, among patients with biopsy-confirmed NASH and F2–F3 fibrosis, semaglutide—a GLP-1 receptor agonist—achieved NASH resolution without worsening fibrosis more often than placebo. This paper does not establish the claimed benefits of pioglitazone or a dual GIP/GLP-1 receptor agonist, or extend its trial finding to people selected by noninvasive tests. Its reported NASH-resolution result also does not, by itself, establish a decrease in hepatic steatosis. (LLM, conf=0.88)
Experimental — accuracy not yet measuredWeight loss achieved with use of GLP-1 RAs and the GIP/GLP-1 RA is beneficial for obstructive sleep apnea, knee osteoarthritis, and metabolic dysfunction-associated steatohepatitis (MASH).
“Weight loss achieved with use of GLP-1 RAs and the GIP/GLP-1 RA is also beneficial for obstructive sleep apnea (132), knee osteoarthritis (133), and metabolic dysfunction–associated steatohepatitis (MASH) (134–136).”
From 13. Older Adults: Standards of Care in Diabetes—2026 (2026) · cites this paper as [136]
The Results (p. 2) report both greater weight loss and more frequent NASH resolution with the GLP-1 receptor agonist semaglutide than with placebo. The Discussion (p. 11) describes weight loss as a potential indirect mechanism, but the trial does not establish that weight loss caused the NASH benefit or evaluate a dual GIP/GLP-1 agonist. This citation supports the MASH-related part of the sentence, not its separately cited sleep-apnea or osteoarthritis claims. (LLM, conf=0.86)
Experimental — accuracy not yet measuredSemaglutide showed a trend for improvements in fibrosis stage.
“semaglutide showed a trend for improvements in fibrosis stage, 82”
From GLP-1 receptor agonists and next-generation incretin-based medications: metabolic, cardiovascular, and renal benefits (2026) · cites this paper as [82]
Pioglitazone therapy, GLP-1 RA therapy, and metabolic surgery have all been shown to reduce NASH activity; pioglitazone therapy and metabolic surgery may also improve hepatic fibrosis.
“Pioglitazone therapy, GLP-1 RA therapy, and metabolic surgery have all been shown to reduce NASH activity; pioglitazone therapy and metabolic surgery may also improve hepatic fi brosis (188,292 -298).”
Studies with semaglutide showed relevant weight losses accompanied by consistent metabolic benefits, and in patients with steatohepatitis a significant increase in the rates of resolution of liver disease.
“Studies conducted with semaglutide showed relevant weight losses, accompanied by consistent metabolic benefits, while investigations in patients with steatohepatitis demonstrated a significant increase in the rates of resolution of liver disease”
From RETATRUTIDE USE IN THE TREATMENT OF METABOLIC DYSFUNCTION-ASSOCIATED STEATOTIC LIVER DISEASE (MASLD) AND OBESITY: AN INTEGRATIVE REVIEW (2026) · cites this paper as NEWSOME et al., 2021
In a 72-week, double-blind phase 2 trial involving 320 patients with biopsy-confirmed NASH and fibrosis stage 1-3, semaglutide showed a significantly higher percentage of patients with NASH resolution (and no worsening of fibrosis) compared to placebo.
“The glucagon‐like peptide‐1 receptor agonist semaglutide has shown a significantly higher percentage of patients with NASH resolution (and no worsening of fibrosis) compared to placebo in a 72‐week, double‐blind phase 2 trial involving 320 patients with biopsy‐confirmed NASH and fibrosis stage 1–340.”
From Current treatment of non‐alcoholic fatty liver disease (2022) · cites this paper as [40]
In that semaglutide trial, improvement in fibrosis stage was seen in 43% of NASH patients and 33% of placebo patients, but this difference was not statistically significant.
“Improvement in fibrosis stage was seen in 43% of NASH patients and 33% of placebo patients, but this difference was not statistically significant [40].”
From Current treatment of non‐alcoholic fatty liver disease (2022) · cites this paper as [40]
In the semaglutide trial, around 38% of patients had no diabetes mellitus, and all had at least a BMI >25.
“around 38% of patients in the study had no (!) diabetes mellitus, however all had at least a BMI >25.”
From Current treatment of non‐alcoholic fatty liver disease (2022) · cites this paper as [40]
No overall improvement in fibrosis grade was detected with liraglutide/semaglutide despite lower reported rates of fibrosis progression for liraglutide.
“However, no overall improvement in fibrosis grade was detected, despite lower reported rates of fibrosis progression for liraglutide [108,109].”
From Obesity and MASLD: Is weight loss the (only) key to treat metabolic liver disease? (2024) · cites this paper as [109]
Semaglutide also reduced inflammation in MASH.
“MASH resolution was mainly driven by improvements in steatosis and ballooning for liraglutide [108], whereas semaglutide also reduced inflammation [109].”
From Obesity and MASLD: Is weight loss the (only) key to treat metabolic liver disease? (2024) · cites this paper as [109]
GLP-1RA treatment with liraglutide and semaglutide results in higher rates of histological MASH resolution without worsening of fibrosis compared to placebo in mixed collectives of people with and without type 2 diabetes.
“Two RCTs with liraglutide and semaglutide in mixed collectives of people with and without type 2 diabetes provided evidence for higher rates of histological MASH resolution without worsening of fibrosis compared to placebo (Table 1).”
From Obesity and MASLD: Is weight loss the (only) key to treat metabolic liver disease? (2024) · cites this paper as [109]
In three 56-week studies of people with obesity and dyslipidemia or hypertension, weight loss ranged from 6.2% to 8.0% with liraglutide 3 mg versus 0.2% to 2.9% with placebo.
“In 3 studies of 56-week duration involving persons with obesity and dyslipidemia or hypertension, weight loss ranged from 6.2% to 8.0% with 3 mg liraglutide vs 0.2% to 2.9% with placebo.754–756”
From American Association of Clinical Endocrinology Clinical Practice Guideline: Developing a Diabetes Mellitus Comprehensive Care Plan-2022 Update. (2022) · cites this paper as [756]
The Patients section (p. 5) describes a semaglutide trial with outcomes assessed at 72 weeks, and the Efficacy section (p. 7) reports weight loss for semaglutide and placebo. Searches for 56-week liraglutide 3-mg studies and the quoted weight-loss ranges found no passage addressing those results. The paper’s different trial does not establish whether the three studies described in the claim occurred. (LLM, conf=0.76)
Experimental — accuracy not yet measuredGrowing evidence supports the positive impact of GLP-1 RAs in reducing hepatic cytolysis enzymes.
“Growing evidence supports the positive impact of GLP-1 RAs in reducing hepatic cytolysis enzymes [56,61,69,70,71,72,73,74,75,76,77,78,79,80,81] (Table 2).”
From GLP-1 Receptor Agonists in Non-Alcoholic Fatty Liver Disease: Current Evidence and Future Perspectives (2023) · cites this paper as [61]
Semaglutide at 0.4 mg/day does not significantly improve fibrosis compared to placebo.
“If semaglutide at a dosage of 0.4 mg/day leads to resolution of steatohepatitis in 59% of cases, no significant difference emerged in the improvement of fibrosis compared to placebo.”
From GLP-1 Receptor Agonists in Non-Alcoholic Fatty Liver Disease: Current Evidence and Future Perspectives (2023) · cites this paper as [61]
GLP-1 RAs significantly improve hepatic steatosis.
“In this regard, GLP-1 RAs have been proven to significantly improve hepatic steatosis.”
From GLP-1 Receptor Agonists in Non-Alcoholic Fatty Liver Disease: Current Evidence and Future Perspectives (2023) · cites this paper as [61]
Improvement in NAS was observed in 83% of patients treated with semaglutide 0.4 mg/day, 80% with 0.2 mg/day, 71% with 0.1 mg/day, and 44% with placebo.
“Furthermore, an improvement in NAS was observed in 83% of patients treated with semaglutide 0.4 mg/day, 80% of those treated with 0.2 mg/day, 71% of those treated with 0.1 mg/day and only 44% of those treated with placebo.”
From GLP-1 Receptor Agonists in Non-Alcoholic Fatty Liver Disease: Current Evidence and Future Perspectives (2023) · cites this paper as [61]
After 72 weeks, semaglutide at 0.4 mg/day results in histological resolution of NASH without progression of fibrosis in 59% of patients, compared with 17% in the placebo group.
“After 72 weeks, treatment with semaglutide at a dose of 0.4 mg/day resulted in the histological resolution of NASH without progression of fibrosis in 59% of patients, compared with 17% in the placebo group.”
From GLP-1 Receptor Agonists in Non-Alcoholic Fatty Liver Disease: Current Evidence and Future Perspectives (2023) · cites this paper as [61]
Semaglutide treatment reduces progression of fibrosis (5% vs 19% in the placebo group).
“However, the treatment was shown to be effective in reducing the progression of fibrosis (5% vs. 19% of the placebo group), in accordance with what previously demonstrated [56].”
From GLP-1 Receptor Agonists in Non-Alcoholic Fatty Liver Disease: Current Evidence and Future Perspectives (2023) · cites this paper as [61]
GLP-1 agonism has promoted NASH resolution in a phase II trial.
“As GLP-1 agonism has promoted NASH resolution in a phase II trial,48”
From An integrated view of anti-inflammatory and antifibrotic targets for the treatment of NASH (2023) · cites this paper as [48]
In adults with biopsy-confirmed NASH and F1-F3 fibrosis, semaglutide 0.4 mg daily versus placebo for 72 weeks improved steatohepatitis resolution without worsening fibrosis, but did not improve fibrosis stage compared with placebo.
“Among adults with biopsy-confirmed NASH and liver fibrosis of stage F1, F2, or F3, semaglutide 0.4 mg s.c.versus placebo daily for 72 weeks improved steatohepatitis resolution with no worsening of fibrosis, but there was no between-group difference in improvement of fibrosis stage.115”
From Management of type 2 diabetes, obesity, or nonalcoholic steatohepatitis with high‐dose GLP‐1 receptor agonists and GLP‐1 receptor‐based co‐agonists (2024) · cites this paper as [115]
In people with MASH (with and without diabetes), semaglutide 0.4 mg once daily for 72 weeks demonstrated that 59% could achieve MASH resolution with no worsening of fibrosis compared to placebo, however there was no improvement in fibrosis stage.
“In people with MASH (with and without diabetes), semaglutide 0.4 mg once daily for 72 weeks demonstrated that 59% of them could achieve MASH resolution with no worsening of fibrosis compared to placebo, however there was not improvement in fibrosis stage [57].”
GLP-1 RAs such as liraglutide 1.8 mg once daily and semaglutide 2.4 mg once weekly have demonstrated benefits in MASH resolution compared to placebo, without however improvement in fibrosis.
“Nevertheless, GLP-1 RAs such as liraglutide 1.8 mg once daily and semaglutide 2.4 mg once weekly have demonstrated their benefits in MASH resolution compared to placebo, without however improvement in fibrosis [57,88].”
GLP-1RA therapies deliver histological benefit in people with MASLD.
“Glucagon-like peptide 1 receptor agonist (GLP-1RA) therapies deliver histological benefit in people with metabolic dysfunction-associated steatotic liver disease (MASLD).”
From Randomised trial comparing weight loss through lifestyle and GLP-1 receptor agonist therapy in people with MASLD (2025) · cites this paper as [16]
Semaglutide achieved resolution of MASH in up to 59% of people and this was associated with a 13% reduction in weight.
“More recently, semaglutide, a more potent GLP1-RA, has achieved resolution of MASH in up to 59% of people and this was associated with a 13% reduction in weight.16”
From Randomised trial comparing weight loss through lifestyle and GLP-1 receptor agonist therapy in people with MASLD (2025) · cites this paper as [16]
The impact of GLP-1RA on liver fibrosis is less clear.
“However, the impact on liver fibrosis is less clear.16,17”
From Randomised trial comparing weight loss through lifestyle and GLP-1 receptor agonist therapy in people with MASLD (2025) · cites this paper as [16]
There is an established body of evidence demonstrating the beneficial impact of GLP-1RA in people with MASLD to decrease hepatic steatosis and resolve MASH.
“There is now an established body of evidence demonstrating the beneficial impact of GLP-1RA in people with MASLD to decrease hepatic steatosis and resolve MASH15,16,30,31”
From Randomised trial comparing weight loss through lifestyle and GLP-1 receptor agonist therapy in people with MASLD (2025) · cites this paper as [16]
GLP-1 receptor agonists have demonstrated efficacy in phase 2 studies with liraglutide and semaglutide.
“of GLP-1 receptor agonists has recently been demonstrated by phase 2 studies with liraglutide194 and semaglutide,195”
From Novel therapeutic targets for cholestatic and fatty liver disease (2022) · cites this paper as [195]
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- Authors
- Newsome, P. N., Buchholtz, K., Cusi, K., Linder, M., Okanoue, T., Ratziu, V., Sanyal, A. J., Sejling, A.-S., & Harrison, S. A.
- Affiliations
- University Hospitals Birmingham NHS Foundation Trust (GB)
- ORCID
- Venue
- New England Journal of Medicine
- Publisher
- Massachusetts Medical Society
- Published
- 2021-03-25
- Volume
- 384
- Issue
- 12
- Pages
- 1113-1124
- ISSN
- 0028-4793 (ISSN-L)
- 1533-4406
- OpenAlex
- W3102426258
- Cited by
- 2,039
- References
- 28
- Citations by year
- 2026: 352 · 2025: 458 · 2024: 417 · 2023: 334 · 2022: 264 · 2021: 205 · 2020: 7 · 2014: 1
- FWCI
- 145.04
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- New England Journal of Medicine (publishedVersion)
- PubMed (publishedVersion)
- HAL (submittedVersion)
- Ghent University Academic Bibliography (Ghent University) (submittedVersion)
- University of Birmingham Research Portal (University of Birmingham) (submittedVersion, other-oa)
- Funders
- Novo Nordisk A/S
- Topics
- Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Keywords
- nonalcoholic steatohepatitis, semaglutide, GLP-1 receptor agonists, liver fibrosis, NASH resolution, weight loss, adverse events, nausea, constipation, vomiting, dose comparison, obesity-related liver disease, drug safety and efficacy, GIP/GLP-1 receptor agonist
- MeSH terms
- Semaglutide, Adolescent, Adult, Aged, Amylases, Biopsy, Diabetes Mellitus, Type 2, Dose-Response Relationship, Drug, Double-Blind Method, Glucagon-Like Peptides, Female, Humans, Injections, Subcutaneous, Lipase, Liver, Liver Cirrhosis, Male, Middle Aged, Young Adult, Non-alcoholic Fatty Liver Disease
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