The DOI matches its Crossref record; 28 of the 28 references it cites were found in a registry or an index.
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.).
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“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]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“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]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“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]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“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]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“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]
Experimental — accuracy not yet measured
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“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]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“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]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“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]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“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]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“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]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“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]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“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]
The cited source says what the claim attributes to it.
In the citing paper
“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).”
The cited source says what the claim attributes to it.
In the citing paper
“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
The cited source says what the claim attributes to it.
In the citing paper
“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]
The cited source says what the claim attributes to it.
In the citing paper
“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]
The cited source says what the claim attributes to it.
In the citing paper
“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]
The cited source says what the claim attributes to it.
In the citing paper
“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]
The cited source says what the claim attributes to it.
In the citing paper
“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]
The cited source says what the claim attributes to it.
In the citing paper
“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]
The check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“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]
Experimental — accuracy not yet measuredIn the citing paper
“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]
In the citing paper
“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]
In the citing paper
“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]
In the citing paper
“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]
In the citing paper
“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]
In the citing paper
“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]
In the citing paper
“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 the citing paper
“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 the citing paper
“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].”
In the citing paper
“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].”
In the citing paper
“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]
In the citing paper
“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]
In the citing paper
“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]
In the citing paper
“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]
In the citing paper
“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]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Design and validation of a histological scoring system for nonalcoholic fatty liver disease†
Kleiner, D. E., Brunt, E. M., Van Natta, M., Behling, C., Contos, M. J., Cummings, O. W., Ferrell, L. D., Liu, Y., Torbenson, M. S., Unalp‐Arida, A., et al. (2005) · Hepatology · doi:10.1002/hep.20701 · Cited by 10,791
Self-citationChalasani, N., Younossi, Z., Lavine, J. E., Charlton, M., Cusi, K., Rinella, M., Harrison, S. A., Brunt, E. M., & Sanyal, A. J. (2018) · Hepatology · doi:10.1002/hep.29367 · Cited by 7,239
Self-citationSemaglutide and Cardiovascular Outcomes in Patients with Type 2 Diabetes
Marso, S. P., Bain, S. C., Consoli, A., Eliaschewitz, F. G., Jódar, E., Leiter, L. A., Lingvay, I., Rosenstock, J., Seufert, J., Warren, M. L., et al. (2016) · New England Journal of Medicine · doi:10.1056/nejmoa1607141 · Cited by 6,900 · cited 1×
“Neoplasms‡ 10 (12) 11 (14) 14 (17) 6 (8)”
EASL–EASD–EASO Clinical Practice Guidelines for the management of non-alcoholic fatty liver disease
(2016) · Journal of Hepatology · doi:10.1016/j.jhep.2015.11.004 · Cited by 4,836
Pioglitazone, Vitamin E, or Placebo for Nonalcoholic Steatohepatitis
Sanyal, A. J., Chalasani, N., Kowdley, K. V., McCullough, A., Diehl, A. M., Bass, N. M., Neuschwander-Tetri, B. A., Lavine, J. E., Tonascia, J., Unalp, A., et al. (2010) · New England Journal of Medicine · doi:10.1056/nejmoa0907929 · Cited by 3,327
Self-citationNeuschwander-Tetri, B. A., Loomba, R., Sanyal, A. J., Lavine, J. E., Van Natta, M. L., Abdelmalek, M. F., Chalasani, N., Dasarathy, S., Diehl, A. M., Hameed, B., et al. (2015) · The Lancet · doi:10.1016/s0140-6736(14)61933-4 · Cited by 2,237
Self-citationArmstrong, M. J., Gaunt, P., Aithal, G. P., Barton, D., Hull, D., Parker, R., Hazlehurst, J. M., Guo, K., Abouda, G., Aldersley, M. A., et al. (2016) · The Lancet · doi:10.1016/s0140-6736(15)00803-x · Cited by 2,203
Self-citationSheka, A. C., Adeyi, O. A., Thompson, J., Hameed, B., Crawford, P. A., & Ikramuddin, S. (2020) · JAMA · doi:10.1001/jama.2020.2298 · Cited by 1,421
Younossi, Z. M., Ratziu, V., Loomba, R., Rinella, M., Anstee, Q. M., Goodman, Z., Bedossa, P., Geier, A., Beckebaum, S., Newsome, P. N., et al. (2019) · The Lancet · doi:10.1016/s0140-6736(19)33041-7 · Cited by 1,277
Self-citationThe Discovery and Development of Liraglutide and Semaglutide
Knudsen, L. B., & Lau, J. (2019) · Frontiers in Endocrinology · doi:10.3389/fendo.2019.00155 · Cited by 970
Flagged first, then by citations
Cited by
Sorted by citations
Items 101–200 of 1,005
Management of non-alcoholic fatty liver disease
Petroni, M. L., Brodosi, L., Bugianesi, E., & Marchesini, G. (2021) · BMJ · doi:10.1136/bmj.m4747 · Cited by 193
Therapeutic landscape of metabolic dysfunction-associated steatohepatitis (MASH)
Do, A., Zahrawi, F. M., & Mehal, W. Z. (2024) · Nature Reviews Drug Discovery · doi:10.1038/s41573-024-01084-2 · Cited by 206
Current therapies and new developments in NASH
Dufour, J., Anstee, Q. M., Bugianesi, E., Harrison, S. A., Loomba, R. S., Paradis, V., Tilg, H., Wong, V. W., & Zelber‐Sagi, S. (2022) · Gut · doi:10.1136/gutjnl-2021-326874 · Cited by 192
Self-citationHarrison, S. A., Browne, S., Suschak, J. J., Tomah, S., Gutierrez, J. A., Yang, J., Roberts, M. S., & Harris, M. S. (2024) · Journal of Hepatology · doi:10.1016/j.jhep.2024.07.006 · Cited by 192
Self-citationGlucagon-like Peptide-1 Receptor-based Therapeutics for Metabolic Liver Disease
Yabut, J. M., & Drucker, D. J. (2022) · Endocrine Reviews · doi:10.1210/endrev/bnac018 · Cited by 189
Nonalcoholic fatty liver disease as a metabolic disease in humans: A literature review
Cariou, B., Byrne, C. D., Loomba, R. S., & Sanyal, A. J. (2021) · Diabetes Obesity and Metabolism · doi:10.1111/dom.14322 · Cited by 187
Self-citationHarrison, S. A., Rolph, T., Knott, M., & Dubourg, J. (2024) · Journal of Hepatology · doi:10.1016/j.jhep.2024.04.034 · Cited by 179
Self-citationKloock, S., Ziegler, C. G., & Dischinger, U. (2023) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2023.108549 · Cited by 173
ElSayed, N. A., Aleppo, G., Bannuru, R. R., Bruemmer, D., Collins, B. S., Cusi, K. J., Ekhlaspour, L., Fleming, T. K., Hilliard, M. E., Johnson, E. L., et al. (2023) · Diabetes Care · doi:10.2337/dc24-s004 · Cited by 173
Self-citationPharmacotherapy of type 2 diabetes: An update and future directions
DeMarsilis, A. J., Reddy, N., Boutari, C., Filippaios, A., Sternthal, E., Katsiki, N., & Mantzoros, C. S. (2022) · Metabolism · doi:10.1016/j.metabol.2022.155332 · Cited by 173
Kanwal, F., Kramer, J. R., Li, L., Yang, Y., Cao, Y., Yu, X., Samuel, R. E., Ali, B., Desiderio, R., Cholankeril, G. T., et al. (2024) · JAMA Internal Medicine · doi:10.1001/jamainternmed.2024.4661 · Cited by 170
Obesity and MASLD: Is weight loss the (only) key to treat metabolic liver disease?
Huttasch, M., Roden, M., & Kahl, S. (2024) · Metabolism · doi:10.1016/j.metabol.2024.155937 · Cited by 169
Burra, P., Bizzaro, D., Gonta, A., Shalaby, S., Gambato, M., Morelli, M. C., Trapani, S., Floreani, A., Marra, F., Brunetto, M. R., et al. (2021) · Liver International · doi:10.1111/liv.14943 · Cited by 165
The Emerging Role of Glucagon-like Peptide-1 Receptor Agonists for the Management of NAFLD
Chavez, C. P., Cusi, K. J., & Kadiyala, S. (2021) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/clinem/dgab578 · Cited by 165
Self-citationFraile, J. M., Palliyil, S., Barelle, C. J., Porter, A. J., & Kovaleva, M. (2021) · Drug Design Development and Therapy · doi:10.2147/dddt.s315724 · Cited by 164
Sangro, P., de la Torre‐Aláez, M., Sangro, B., & D’Avola, D. (2023) · Journal of Physiology and Biochemistry · doi:10.1007/s13105-023-00954-4 · Cited by 163
Portincasa, P., Khalil, M., Mahdi, L., Perniola, V., Idone, V., Graziani, A., Baffy, G., & Ciaula, A. D. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25115640 · Cited by 167
Signaling pathways in macrophages: molecular mechanisms and therapeutic targets
Li, M., Wang, M., Wen, Y., Zhang, H., Zhao, G., & Gao, Q. (2023) · MedComm · doi:10.1002/mco2.349 · Cited by 165
Kokkorakis, M., Boutari, C., Hill, M. A., Kotsis, V., Loomba, R., Sanyal, A. J., & Mantzoros, C. S. (2024) · Metabolism · doi:10.1016/j.metabol.2024.155835 · Cited by 155
Self-citationNewsome, P. N., Sanyal, A. J., Engebretsen, K. A., Kliers, I., Østergaard, L., Vanni, D. S., Bugianesi, E., Rinella, M. E., Roden, M., & Ratziu, V. (2024) · Alimentary Pharmacology & Therapeutics · doi:10.1111/apt.18331 · Cited by 155
Self-citationCelletti, F., Farrar, J., & De Regil, L. (2026) · JAMA · doi:10.1001/jama.2025.24288 · Cited by 153
Theodorakis, N., & Nikolaou, M. (2025) · Biomolecules · doi:10.3390/biom15020213 · Cited by 149
Harrison, S. A., Abdelmalek, M. F., Neff, G., Gunn, N., Guy, C. D., Alkhouri, N., Bashir, M. R., Freilich, B., Kohli, A., Khazanchi, A., et al. (2022) · The Lancet. Gastroenterology & hepatology · doi:10.1016/s2468-1253(22)00017-6 · Cited by 148
Self-citationLipid metabolism in MASLD and MASH: From mechanism to the clinic
Carli, F., Della Pepa, G., Sabatini, S., Vidal Puig, A., & Gastaldelli, A. (2024) · JHEP Reports · doi:10.1016/j.jhepr.2024.101185 · Cited by 147
Prevention of NAFLD-associated HCC: Role of lifestyle and chemoprevention
Lange, N. F., Radu, P., & Dufour, J. (2021) · Journal of Hepatology · doi:10.1016/j.jhep.2021.07.025 · Cited by 144
Calvo, S. S.-C., Bharath, L. P., Pugh, G. H., SantaCruz-Calvo, L., Lenin, R. R., Lutshumba, J., Liu, R., Bachstetter, A. D., Zhu, B., & Nikolajczyk, B. S. (2021) · Nature Reviews Endocrinology · doi:10.1038/s41574-021-00575-1 · Cited by 149
Clinical Trial Landscape in NASH
Harrison, S. A., Loomba, R. S., Dubourg, J., Ratziu, V., & Noureddin, M. (2023) · Clinical Gastroenterology and Hepatology · doi:10.1016/j.cgh.2023.03.041 · Cited by 142
Self-citationTherapeutic management of metabolic dysfunction associated steatotic liver disease
Zeng, J., Fan, J., & Francque, S. (2024) · United European Gastroenterology Journal · doi:10.1002/ueg2.12525 · Cited by 142
Nadolsky, K., Garvey, W. T., Agarwal, M., Bonnecaze, A., Burguera, B., Chaplin, M. D., Griebeler, M. L., Harris, S. R., Schellinger, J. N., Simonetti, J., et al. (2025) · Endocrine Practice · doi:10.1016/j.eprac.2025.07.017 · Cited by 141
Mantovani, A., Petracca, G., Csermely, A., Beatrice, G., & Targher, G. (2020) · Metabolites · doi:10.3390/metabo11010022 · Cited by 141
Alexopoulos, A., Crowley, M. J., Wang, Y., Moylan, C. A., Guy, C. D., Henao, R., Piercy, D. L., Seymour, K. A., Sudan, R., Portenier, D. D., et al. (2021) · Hepatology · doi:10.1002/hep.31806 · Cited by 141
Derivatization with fatty acids in peptide and protein drug discovery
Kurtzhals, P., Østergaard, S., Nishimura, E., & Kjeldsen, T. (2022) · Nature Reviews Drug Discovery · doi:10.1038/s41573-022-00529-w · Cited by 139
Wong, C. K., Yusta, B., Koehler, J. A., Baggio, L. L., McLean, B. A., Matthews, D., Seeley, R. J., & Drucker, D. J. (2022) · Cell Metabolism · doi:10.1016/j.cmet.2022.08.003 · Cited by 138
Harrison, S. A., Gunn, N., Neff, G. W., Kohli, A., Liu, L., Flyer, A., Goldkind, L., & Bisceglie, A. M. D. (2021) · Nature Communications · doi:10.1038/s41467-021-25701-5 · Cited by 137
Self-citationMASLD and the Development of HCC: Pathogenesis and Therapeutic Challenges
Phoolchund, A. G. S., & Khakoo, S. I. (2024) · Cancers · doi:10.3390/cancers16020259 · Cited by 137
Castera, L., Laouenan, C., Vallet-Pichard, A., Vidal-Trécan, T., Manchon, P., Paradis, V., Roulot, D., Gault, N., Boitard, C., Terris, B., et al. (2023) · Diabetes Care · doi:10.2337/dc22-2048 · Cited by 136
Wang, L., Berger, N. A., Kaelber, D. C., & Xu, R. (2024) · Gastroenterology · doi:10.1053/j.gastro.2024.04.029 · Cited by 136
New and emerging treatments for metabolic dysfunction-associated steatohepatitis
Tincopa, M. A., Anstee, Q. M., & Loomba, R. S. (2024) · Cell Metabolism · doi:10.1016/j.cmet.2024.03.011 · Cited by 135
Intestinal dysbiosis in nonalcoholic fatty liver disease (NAFLD): focusing on the gut–liver axis
Han, H. L., Jiang, Y., Wang, M., Melaku, M., Liu, L., Zhao, Y. M., Everaert, N., Yi, B., & Zhang, H. (2021) · Critical Reviews in Food Science and Nutrition · doi:10.1080/10408398.2021.1966738 · Cited by 135
Breakthroughs in therapies for NASH and remaining challenges
Ratziu, V., Francque, S., & Sanyal, A. (2022) · Journal of Hepatology · doi:10.1016/j.jhep.2022.04.002 · Cited by 132
Self-citationThe Role of the Gut-Liver Axis in Metabolic Dysfunction-Associated Fatty Liver Disease
Martín‐Mateos, R., & Albillos, A. (2021) · Frontiers in Immunology · doi:10.3389/fimmu.2021.660179 · Cited by 132
Glucagon-Like Peptide-1: New Regulator in Lipid Metabolism
Bu, T., Sun, Z., Pan, Y., Deng, X., & Yuan, G. (2024) · Diabetes & Metabolism Journal · doi:10.4093/dmj.2023.0277 · Cited by 131
Takeshita, Y., Honda, M., Harada, K., Kita, Y., Takata, N., Tsujiguchi, H., Tanaka, T., Goto, H., Nakano, Y., Iida, N., et al. (2022) · Diabetes Care · doi:10.2337/dc21-2049 · Cited by 131
Miller, D. M., McCauley, K. F., & Dunham‐Snary, K. J. (2025) · Endocrinology Diabetes & Metabolism · doi:10.1002/edm2.70132 · Cited by 131
Metabolic dysfunction-associated steatotic liver disease and the heart
Driessen, S., Francque, S., Anker, S. D., Cabezas, M. C., Grobbee, D. E., Tushuizen, M. E., & Holleboom, A. G. (2023) · Hepatology · doi:10.1097/hep.0000000000000735 · Cited by 133
Kim, G., Moon, J. H., & Kim, W. K. (2023) · Clinical and Molecular Hepatology · doi:10.3350/cmh.2023.0277 · Cited by 128
Preparing for the NASH Epidemic: A Call to Action
Kanwal, F., Shubrook, J. H., Younossi, Z. M., Natarajan, Y., Bugianesi, E., Rinella, M. E., Harrison, S. A., Mantzoros, C. S., Pfotenhauer, K. M., Klein, S., et al. (2021) · Gastroenterology · doi:10.1053/j.gastro.2021.04.074 · Cited by 127
Self-citationGLP-1 physiology in obesity and development of incretin-based drugs for chronic weight management
Holst, J. J. (2024) · Nature Metabolism · doi:10.1038/s42255-024-01113-9 · Cited by 125
Byrne, C. D., & Targher, G. (2021) · Diabetes Obesity and Metabolism · doi:10.1111/dom.14484 · Cited by 125
Sun, Q., Xing, X., Wang, H., Wan, K., Fan, R., Liu, C., Wang, Y., Wu, W., Wang, Y., & Wang, R. (2023) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2023.115586 · Cited by 125
Habibullah, M., Jemmieh, K., Ouda, A., Haider, M. Z., Malki, M. I., & Elzouki, A.-N. Y. (2024) · Frontiers in Medicine · doi:10.3389/fmed.2024.1291501 · Cited by 129
Nauck, M. A., Tuttle, K. R., Tschöp, M. H., & Blüher, M. (2026) · The Lancet · doi:10.1016/s0140-6736(25)02105-1 · Cited by 123
EDP-305 in patients with NASH: a phase II double-blind placebo-controlled dose-ranging study
Ratziu, V., Rinella, M. E., Neuschwander-Tetri, B. A., Lawitz, E., Denham, D., Kayali, Z., Sheikh, A., Kowdley, K. V., Desta, T., Elkhashab, M., et al. (2022) · Journal of Hepatology · doi:10.1016/j.jhep.2021.10.018 · Cited by 123
Self-citationLoomba, R. S., Bédossa, P., Grimmer, K., Kemble, G. W., Martins, E. B., McCulloch, W. F., O’Farrell, M., Tsai, W.-W., Cobiella, J., Lawitz, E., et al. (2024) · The Lancet. Gastroenterology & hepatology · doi:10.1016/s2468-1253(24)00246-2 · Cited by 123
Self-citationPharmacologic inhibition of lipogenesis for the treatment of NAFLD
Esler, W. P., & Cohen, D. E. (2023) · Journal of Hepatology · doi:10.1016/j.jhep.2023.10.042 · Cited by 122
Personalized type 2 diabetes management: an update on recent advances and recommendations
Williams, D. M., Jones, H., & Stephens, J. W. (2022) · Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy · doi:10.2147/dmso.s331654 · Cited by 121
Targher, G., Mantovani, A., & Byrne, C. D. (2023) · The Lancet Gastroenterology & Hepatology · doi:10.1016/s2468-1253(22)00338-7 · Cited by 121
Yang, Z., Lv, Y., Yu, M., Mei, M., Xiang, L., Zhao, S., & Li, R. (2022) · Frontiers in Pharmacology · doi:10.3389/fphar.2022.925377 · Cited by 120
Ratziu, V., Scanlan, T. S., & Bruinstroop, E. (2024) · Journal of Hepatology · doi:10.1016/j.jhep.2024.10.018 · Cited by 118
Self-citationHarrison, S. A., Frías, J. P., Lucas, K. J., Reiss, G. M., Neff, G. W., Bollepalli, S., Su, Y., Chan, D. C., Tillman, E. J., Moulton, A. W., et al. (2024) · Clinical Gastroenterology and Hepatology · doi:10.1016/j.cgh.2024.02.022 · Cited by 117
Self-citationGlucagon-Like Peptide 1 Receptor Agonists and Mental Health: A Systematic Review and Meta-Analysis
Pierret, A. C. S., Mizuno, Y., Saunders, P., Lim, E., De Giorgi, R., Howes, O. D., McCutcheon, R. A., McGowan, B., Sen Gupta, P., Smith, D., et al. (2025) · JAMA Psychiatry · doi:10.1001/jamapsychiatry.2025.0679 · Cited by 116
Risk of Heart Failure in Patients With Nonalcoholic Fatty Liver Disease
Mantovani, A., Byrne, C. D., Benfari, G., Bonapace, S., Simon, T. G., & Targher, G. (2022) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2021.11.007 · Cited by 115
Lau, H. C.-H., Zhang, X., & Yu, J. (2025) · Nature Reviews Gastroenterology & Hepatology · doi:10.1038/s41575-025-01089-1 · Cited by 126
de Souza, M. H. G., Al‐Sharif, L., Antunes, V., Huang, D. Q., & Loomba, R. (2025) · Hepatology · doi:10.1097/hep.0000000000001254 · Cited by 114
Drożdż, K., Nabrdalik, K., Hajzler, W., Kwiendacz, H., Gumprecht, J., & Lip, G. Y. H. (2021) · Nutrients · doi:10.3390/nu14010103 · Cited by 115
Kreiner, F. F., Kraaijenhof, J. M., von Herrath, M., Hovingh, G. K., & von Scholten, B. J. (2022) · Expert Review of Clinical Immunology · doi:10.1080/1744666x.2022.2045952 · Cited by 115
Qi, X., Li, J., Caussy, C., Teng, G., & Loomba, R. (2024) · Hepatology · doi:10.1097/hep.0000000000000913 · Cited by 113
Byrne, C. D., Armandi, A., Pellegrinelli, V., Vidal‐Puig, A., & Bugianesi, E. (2025) · Nature Reviews Gastroenterology & Hepatology · doi:10.1038/s41575-025-01045-z · Cited by 113
Min, J. S., Jo, S. J., Lee, S., Kim, D. Y., Kim, D. H., Lee, C. B., & Bae, S. K. (2025) · Drug Design Development and Therapy · doi:10.2147/dddt.s506957 · Cited by 116
Muthiah, M. D., Han, N. C., & Sanyal, A. J. (2021) · Diabetes Obesity and Metabolism · doi:10.1111/dom.14521 · Cited by 111
Self-citationJara, M., Norlin, J., Kjær, M. S., Almholt, K., Bendtsen, K. M., Bugianesi, E., Cusi, K. J., Galsgaard, E. D., Geybels, M. S., Gluud, L. L., et al. (2025) · Nature Medicine · doi:10.1038/s41591-025-03799-0 · Cited by 114
Self-citationMahapatra, M. K., Karuppasamy, M., & Sahoo, B. M. (2022) · Pharmaceutical Research · doi:10.1007/s11095-022-03302-1 · Cited by 110
Review article: therapeutic aspects of bile acid signalling in the gut‐liver axis
Simbrunner, B., Trauner, M., & Reiberger, T. (2021) · Alimentary Pharmacology & Therapeutics · doi:10.1111/apt.16602 · Cited by 108
Relationship of Nonalcoholic Fatty Liver Disease and Heart Failure With Preserved Ejection Fraction
Salah, H. M., Pandey, A., Soloveva, A. E., Abdelmalek, M. F., Diehl, A. M., Moylan, C. A., Wegermann, K., Rao, V. N., Hernandez, A. F., Tedford, R. J., et al. (2021) · JACC Basic to Translational Science · doi:10.1016/j.jacbts.2021.07.010 · Cited by 110
Roeb, E., Canbay, A. E., Tacke, F., Bantel, H., Bojunga, J., de Laffolie, J., Demir, M., Denzer, U. W., Geier, A., Hofmann, W. P., et al. (2022) · Zeitschrift für Gastroenterologie · doi:10.1055/a-1880-2283 · Cited by 108
Huang, S., & Liu, C. (2023) · Clinical and Molecular Hepatology · doi:10.3350/cmh.2022.0422 · Cited by 108
The Molecular Mechanisms of Liver Fibrosis and Its Potential Therapy in Application
Zhang, D., Zhang, Y., & Sun, B. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms232012572 · Cited by 107
Duseja, A. K., Singh, S. P., De, A., Madan, K., Rao, P. N., Shukla, A., Choudhuri, G., Saigal, S., Shalimar, S., Arora, A., et al. (2022) · Journal of Clinical and Experimental Hepatology · doi:10.1016/j.jceh.2022.11.014 · Cited by 107
The pathophysiology of MASLD: an immunometabolic perspective
Schwärzler, J., Grabherr, F., Grander, C., Adolph, T. E., & Tilg, H. (2023) · Expert Review of Clinical Immunology · doi:10.1080/1744666x.2023.2294046 · Cited by 107
Non-Alcoholic Fatty Liver Disease in Lean and Non-Obese Individuals: Current and Future Challenges
Kuchay, M. S., Martínez‐Montoro, J. I., Choudhary, N. S., Fernández‐García, J. C., & Ramos‐Molina, B. (2021) · Biomedicines · doi:10.3390/biomedicines9101346 · Cited by 105
The Link between NAFLD and Metabolic Syndrome
Radu, F., Potcovaru, C.-G., Salmen, T., Filip, P. V., Pop, C. S., & Fierbinteanu-Braticevici, C. G. (2023) · Diagnostics · doi:10.3390/diagnostics13040614 · Cited by 104
Ratziu, V., Hompesch, M., Petitjean, M., Serdjebi, C., Iyer, J. S., Parwani, A. V., Tai, D., Bugianesi, E., Cusi, K. J., Friedman, S. L., et al. (2023) · Journal of Hepatology · doi:10.1016/j.jhep.2023.10.015 · Cited by 103
Self-citationGLP-1a: Going beyond Traditional Use
Laurindo, L. F., Barbalho, S. M., Guiguer, E. L., da Silva Soares de Souza, M., de Souza, G. A., Fidalgo, T. M., Araújo, A. C., de Souza Gonzaga, H. F., de Bortoli Teixeira, D., de Oliveira Silva Ullmann, T., et al. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23020739 · Cited by 102
Glucagon-like peptide 1 receptor is a T cell-negative costimulatory molecule
Ben Nasr, M., Usuelli, V., Dellepiane, S., Seelam, A. J., Fiorentino, T. V., D’Addio, F., Fiorina, E., Xu, C., Xie, Y., Balasubramanian, H. B., et al. (2024) · Cell Metabolism · doi:10.1016/j.cmet.2024.05.001 · Cited by 102
Inflammatory and fibrotic mechanisms in NAFLD—Implications for new treatment strategies
Lee, Y. A., & Friedman, S. L. (2021) · Journal of Internal Medicine · doi:10.1111/joim.13380 · Cited by 104
Lipotoxicity-driven metabolic dysfunction-associated steatotic liver disease (MASLD)
Iturbe-Rey, S., Maccali, C., Arrese, M. A., Aspichueta, P., de Oliveira, C. P. M. S., Castro, R. E., Lapitz, A., Izquierdo‐Sánchez, L., Bujanda, L., Perugorria, M. J., et al. (2024) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2024.119053 · Cited by 102
GLP1 Receptor Agonists—Effects beyond Obesity and Diabetes
Wilbon, S. S., & Kolonin, M. G. (2023) · Cells · doi:10.3390/cells13010065 · Cited by 101
Gastaldelli, A., Sabatini, S., Carli, F., Gaggini, M., Bril, F., Belfort‐DeAguiar, R., Positano, V., Barb, D., Kadiyala, S., Harrison, S., et al. (2021) · Liver International · doi:10.1111/liv.15005 · Cited by 101
Self-citationMuzurović, E. M., Volčanšek, Š., Zibar, K., Janež, A., Mikhailidis, D. P., Rizzo, M., & Mantzoros, C. S. (2022) · Journal of Cardiovascular Pharmacology and Therapeutics · doi:10.1177/10742484221146371 · Cited by 101
Abushamat, L. A., Shah, P. A., Eckel, R. H., Harrison, S. A., & Barb, D. (2024) · Clinical Gastroenterology and Hepatology · doi:10.1016/j.cgh.2024.01.032 · Cited by 103
Self-citationCiardullo, S., Muraca, E., Vergani, M., Invernizzi, P., & Perseghin, G. (2023) · Gastroenterology report · doi:10.1093/gastro/goae029 · Cited by 101
Helmstädter, J., Keppeler, K., Küster, L., Münzel, T., Daiber, A., & Steven, S. (2022) · British Journal of Pharmacology · doi:10.1111/bph.15462 · Cited by 99
Simon, T. G., Patorno, E., & Schneeweiss, S. (2022) · Clinical Gastroenterology and Hepatology · doi:10.1016/j.cgh.2021.07.010 · Cited by 98
Ghosal, S., Datta, D., & Sinha, B. (2021) · Scientific Reports · doi:10.1038/s41598-021-01663-y · Cited by 98
Vosoughi, K., Atieh, J., Khanna, L., Khoshbin, K., Prokop, L. J., Davitkov, P., Murad, M. H., & Camilleri, M. (2021) · eClinicalMedicine · doi:10.1016/j.eclinm.2021.101213 · Cited by 97
Current Options and Future Directions for NAFLD and NASH Treatment
Zhang, C., & Yang, M. J. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22147571 · Cited by 97
Zhang, X., Lau, H. C.-H., & Yu, J. Q. (2025) · Pharmacological Reviews · doi:10.1016/j.pharmr.2024.100018 · Cited by 100
Ndumele, C. E., Rodríguez, F., Dixon, D. L., Khan, S. S., Mukherjee, D., Bajaj, M. S., Bangalore, S., Bozkurt, B., Breathett, K. K., Clarke, S. L., et al. (2026) · Circulation · doi:10.1161/cir.0000000000001453 · Cited by 101
Harrison, S. A., Thang, C., Bolze, S., Dewitt, S., Hallakou-Bozec, S., Dubourg, J., Bedossa, P., Cusi, K., Ratziu, V., Grouin, J.-M., et al. (2023) · Journal of Hepatology · doi:10.1016/j.jhep.2023.02.004 · Cited by 96
Self-citationThe Multifaceted Roles of Macrophages in NAFLD Pathogenesis
Vonderlin, J., Chavakis, T., Sieweke, M., & Tacke, F. (2023) · Cellular and Molecular Gastroenterology and Hepatology · doi:10.1016/j.jcmgh.2023.03.002 · Cited by 96
Metadata
- 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
- 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 › Hepatology › 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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review