Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 3 complete abstracts (675 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
Lipid infiltration of the hepatic parenchymal cells resulting in a yellow-colored liver. The abnormal lipid accumulation is usually in the form of triglycerides, either as a single large droplet or multiple small droplets. Fatty liver is caused by an imbalance in the metabolism of fatty acids.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Liver, Fatty; Hepatic Steatosis; Hepatosteatosis; Steatohepatitis; Steatohepatitides; Liver Steatosis; Liver Steatoses; Steatoses, Liver.
Where it fits in the MeSH classification
- Broader topics
- Liver Diseases
- Narrower topics
- Fatty Liver, Alcoholic; Non-alcoholic Fatty Liver Disease; Reye Syndrome
Related concepts
- Triglycerides
- Fatty Acids
Research landscape
PubMed indexes 60,269 records tagged with the MeSH heading “Fatty Liver” (counts retrieved 2026-11-04). 27,056 of them (44.9%) were published from 2020 onward, and the busiest period so far is 2020 onward with 27,056 records.
Reviews account for 10,203 records (16.9%) and meta-analyses for 1,150. Randomized controlled trials number 1,295 (2.1%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 7,224 |
| 2000-2009 | 5,903 |
| 2010-2019 | 20,086 |
| 2020 onward | 27,056 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 10,203 | 16.9% |
| Meta-analyses | 1,150 | 1.9% |
| Randomized controlled trials | 1,295 | 2.1% |
Method: PubMed query "Fatty Liver"[MeSH Terms] with publication-type and date filters, retrieved 2026-11-04.
Reading the evidence in digestive system and liver
Gut and liver research ranges from laboratory studies of the microbiome to large trials of drugs and surgery. Symptoms such as pain, reflux or bowel change are reported by patients and overlap between conditions, and diet and microbiome studies are mostly observational. Check whether the study measured symptoms, tissue findings or long-term outcomes, how the diagnosis was made and how long people were followed. Nothing here replaces advice from a qualified clinician.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Prospective validation of imaging and serum diagnostic biomarkers of steatohepatitis and fibrosis in MASLD: the LITMUS Imaging Study | 2026 | Research article Design not recorded in structured metadata | 6 | cc by PMID 42498741 · DOI · PMC13472969 |
| Cardiolipin deficiency disrupts electron transport chain and drives steatohepatitis | 2026 | Research article Design not recorded in structured metadata | 5 | cc by PMID 42684124 · DOI · PMC13537762 |
| GLP-1 RA Plus SGLT2i Versus Monotherapy in MASLD and Type 2 Diabetes: Three Pairwise Target Trial Emulations | 2026 | Research article Design not recorded in structured metadata | 4 | cc by PMID 42442720 · DOI · PMC13534337 |
Prospective validation of imaging and serum diagnostic biomarkers of steatohepatitis and fibrosis in MASLD: the LITMUS Imaging Study [1]
Abstract reading summary — source excerpts
- Opening excerpt
- There is a need for robust evaluations of noninvasive biomarkers for metabolic dysfunction-associated steatotic liver disease.
- Closing excerpt
- Serum biomarkers tended to outperform imaging for identifying at-risk MASH, whereas elastography and composite scores showed excellent accuracy for staging advanced fibrosis and cirrhosis.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (272 words)
There is a need for robust evaluations of noninvasive biomarkers for metabolic dysfunction-associated steatotic liver disease. This prospective multicenter study assessed the diagnostic accuracy of imaging (including liver stiffness measurement (LSM) using magnetic resonance elastography (MRE) and FibroScan (vibration-controlled transient elastography (VCTE)), serum biomarkers (including NIS2+) and composite scores (including Agile 3+ and Agile 4) for centrally read steatohepatitis and fibrosis. For cirrhosis, several biomarkers exceeded the minimum acceptable performance criterion (MAC), including MRE (area under the receiver operating curve (AUC) 0.91; P < 0.01), VCTE-LSM (AUC 0.87; P < 0.01), Agile 3+ (AUC 0.89; P < 0.01) and Agile 4 (AUC 0.88; P < 0.01). Among 357 participants, fibrosis stages F0-F4 were present in 12%, 16%, 25%, 32% and 15%, respectively. NIS2+ had the highest diagnostic accuracy among serum biomarkers for metabolic dysfunction-associated steatohepatitis (MASH; AUC 0.83) and at-risk MASH (MASH with at least stage 2 fibrosis; AUC 0.82), although neither significantly exceeded the MAC (P = 0.15 and P = 0.19). Among imaging biomarkers, MRE showed the highest performance for MASH (AUC 0.71) and at-risk MASH (AUC 0.75), but these remained below the MAC. For fibrosis staging, performance was stronger: MRE met the MAC for advanced fibrosis (AUC 0.91; P < 0.01), as did Agile 3+ (AUC 0.84; P = 0.03). For cirrhosis, several biomarkers exceeded the MAC, including MRE (AUC 0.91; P < 0.01), VCTE-LSM (AUC 0.87; P < 0.01), Agile 3+ (AUC 0.89; P < 0.01) and Agile 4 (AUC 0.88; P < 0.01). Serum biomarkers tended to outperform imaging for identifying at-risk MASH, whereas elastography and composite scores showed excellent accuracy for staging advanced fibrosis and cirrhosis.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42498741 · DOI · PMC13472969
Cardiolipin deficiency disrupts electron transport chain and drives steatohepatitis [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Metabolic dysfunction-associated steatotic liver disease (MASLD) is a progressive disorder marked by lipid accumulation, leading to metabolic dysfunction-associated steatohepatitis (MASH).
- Closing excerpt
- Thus, low mitochondrial CL disrupts the ETC to promote oxidative stress and contributes to the pathogenesis of MASH.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (158 words)
Metabolic dysfunction-associated steatotic liver disease (MASLD) is a progressive disorder marked by lipid accumulation, leading to metabolic dysfunction-associated steatohepatitis (MASH). A key feature of the transition to MASH involves oxidative stress resulting from defects in mitochondrial oxidative phosphorylation (OXPHOS). Here, we show that pathological alterations in the lipid composition of the inner mitochondrial membrane (IMM) directly instigate electron transfer inefficiency to promote oxidative stress. Specifically, mitochondrial cardiolipin (CL) was downregulated with MASLD/MASH in humans and in mice. Hepatocyte-specific CL synthase knockout (CLS-LKO) led to spontaneous and robust MASH with extensive steatotic and fibrotic phenotype. Loss of CL paradoxically increased mitochondrial respiratory capacity but also promoted electron leak primarily at sites IIIQO and IIF of the electron transport chain (ETC), reduced the formation of I + III2 + IV respiratory supercomplex, and disrupted the propensity of coenzyme Q to become reduced. Thus, low mitochondrial CL disrupts the ETC to promote oxidative stress and contributes to the pathogenesis of MASH.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42684124 · DOI · PMC13537762
GLP-1 RA Plus SGLT2i Versus Monotherapy in MASLD and Type 2 Diabetes: Three Pairwise Target Trial Emulations [3]
Abstract reading summary — source excerpts
- Opening excerpt
- IntroductionGlucagon-like peptide-1 receptor agonists (GLP-1 RAs) and sodium-glucose cotransporter-2 inhibitors (SGLT2is) have demonstrated cardiovascular and metabolic benefits individually; however, the comparative effectiveness of combination therapy versus monotherapy in patients with metabolic dysfunction-associated steatotic liver disease (MASLD) and type 2 diabetes mellitus (T2DM) remains incompletely characterized.
- Closing excerpt
- ConclusionsGLP-1 RA and SGLT2i combination therapy significantly reduced mortality and liver outcomes versus SGLT2i monotherapy in MASLD with T2DM; however, increased MACE risk versus GLP-1 RA monotherapy warrants consideration in management decisions.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (245 words)
IntroductionGlucagon-like peptide-1 receptor agonists (GLP-1 RAs) and sodium-glucose cotransporter-2 inhibitors (SGLT2is) have demonstrated cardiovascular and metabolic benefits individually; however, the comparative effectiveness of combination therapy versus monotherapy in patients with metabolic dysfunction-associated steatotic liver disease (MASLD) and type 2 diabetes mellitus (T2DM) remains incompletely characterized.MethodsWe conducted three pairwise target trial emulations using the TriNetX Research Network. Adults with MASLD and T2DM initiating GLP-1 RA plus SGLT2i combination therapy, GLP-1 RA monotherapy, or SGLT2i monotherapy were identified. Primary outcomes were all-cause mortality, major adverse cardiovascular events (MACE), and composite liver outcomes. Propensity score matching (PSM) (1:1) was performed for each pairwise comparison. Cox proportional hazards regression with Bayesian hierarchical bias-effect (BHBE) correction was utilized to address residual confounding.ResultsFollowing PSM, 42423 combination versus 42 423 GLP-1 RA, 40349 combination versus 40 349 SGLT2i, and 51 826 GLP-1 RA versus 51 826 SGLT2i patients were analyzed. Combination therapy significantly reduced all-cause mortality versus SGLT2i monotherapy (hazard ratio [HR] 0.522, 95% confidence interval [CI] 0.488-0.559), with probable benefit after bias correction (corrected HR 0.655, posterior probability 92.4%; credible interval includes the null). Combination therapy demonstrated increased MACE risk versus GLP-1 RA (HR 1.106, 95% CI 1.045-1.170), remaining significant after correction (corrected HR 1.111). Composite liver outcomes favored combination therapy versus SGLT2i (corrected HR 0.907, probability of benefit 81.9%).ConclusionsGLP-1 RA and SGLT2i combination therapy significantly reduced mortality and liver outcomes versus SGLT2i monotherapy in MASLD with T2DM; however, increased MACE risk versus GLP-1 RA monotherapy warrants consideration in management decisions.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42442720 · DOI · PMC13534337
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article The Global Epidemiology of Nonalcoholic Fatty Liver Disease and Nonalcoholic Steatohepatitis Among Patients With Type 2 Diabetes [4]
- Research article Global prevalence of non-alcoholic fatty liver disease in type 2 diabetes mellitus: an updated systematic review and meta-analysis [5]
- Research article Global incidence of non-alcoholic fatty liver disease: A systematic review and meta-analysis of 63 studies and 1,201,807 persons [6]
- Research article Genome-wide association meta-analysis identifies 17 loci associated with nonalcoholic fatty liver disease [7]
- Research article Performance of non-invasive tests and histology for the prediction of clinical outcomes in patients with non-alcoholic fatty liver disease: an individual participant data meta-analysis [8]
- Research article Type 2 diabetes, hepatic decompensation, and hepatocellular carcinoma in patients with non-alcoholic fatty liver disease: an individual participant-level data meta-analysis [9]
Full-text reviews on EvidenceLib
Open-access review articles about this topic, reproduced in full with authors, licence and references.
Non-alcoholic fatty liver disease and coexisting depression, anxiety and/or stress in adults: a systematic review and meta-analysis
Sue Shea, Christos Lionis, Chris Kite et al. · Frontiers in Endocrinology 2024 · CC BY 4.0
Does the Mediterranean Diet Have Any Effect on Lipid Profile, Central Obesity and Liver Enzymes in Non-Alcoholic Fatty Liver Disease (NAFLD) Subjects? A Systematic Review and Meta-Analysis of Randomized Control Trials
Cristian Del Bo’, Simone Perna, Sabika Allehdan et al. · Nutrients 2023 · CC BY 4.0
Risk of non-alcoholic fatty liver disease in patients with chronic plaque psoriasis: an updated systematic review and meta-analysis of observational studies
F Bellinato, P Gisondi, A Mantovani et al. · Journal of Endocrinological Investigation 2022 · CC BY 4.0
Endothelial Cell Dysfunction and Nonalcoholic Fatty Liver Disease (NAFLD): A Concise Review
Narjes Nasiri-Ansari, Theodoros Androutsakos, Christina-Maria Flessa et al. · Cells 2022 · CC BY 4.0
A meta-analysis of the effects of glucagon-like-peptide 1 receptor agonist (GLP1-RA) in nonalcoholic fatty liver disease (NAFLD) with type 2 diabetes (T2D)
Samit Ghosal, Debasis Datta, Binayak Sinha · Scientific Reports 2021 · CC BY 4.0
References
- Pavlides M, Vali Y, Mózes FE, Wonders K, Akhtar S, Hockings PD, et al.. Prospective validation of imaging and serum diagnostic biomarkers of steatohepatitis and fibrosis in MASLD: the LITMUS Imaging Study. . 2026. PMID 42498741 · DOI · PMC13472969
- Brothwell MJ, Cao G, Maschek JA, Poss AM, Peterlin AD, Wang L, et al.. Cardiolipin deficiency disrupts electron transport chain and drives steatohepatitis. . 2026. PMID 42684124 · DOI · PMC13537762
- Alkuwaiti MA, Al-Harbi FA, Alsaif AK, AlSughayyir ZM, Alsaud RS, Aljabr MN, et al.. GLP-1 RA Plus SGLT2i Versus Monotherapy in MASLD and Type 2 Diabetes: Three Pairwise Target Trial Emulations. . 2026. PMID 42442720 · DOI · PMC13534337
- Younossi ZM, Golabi P, Price JK, Owrangi S, Gundu-Rao N, Satchi R, et al.. The Global Epidemiology of Nonalcoholic Fatty Liver Disease and Nonalcoholic Steatohepatitis Among Patients With Type 2 Diabetes. Clin Gastroenterol Hepatol. 2024. PMID 38521116 · DOI
- En Li Cho E, Ang CZ, Quek J, Fu CE, Lim LKE, Heng ZEQ, et al.. Global prevalence of non-alcoholic fatty liver disease in type 2 diabetes mellitus: an updated systematic review and meta-analysis. Gut. 2023. PMID 37491159 · DOI
- Le MH, Le DM, Baez TC, Wu Y, Ito T, Lee EY, et al.. Global incidence of non-alcoholic fatty liver disease: A systematic review and meta-analysis of 63 studies and 1,201,807 persons. J Hepatol. 2023. PMID 37040843 · DOI
- Chen Y, Du X, Kuppa A, Feitosa MF, Bielak LF, O'Connell JR, et al.. Genome-wide association meta-analysis identifies 17 loci associated with nonalcoholic fatty liver disease. Nat Genet. 2023. PMID 37709864 · DOI · PMC10918428
- Mózes FE, Lee JA, Vali Y, Alzoubi O, Staufer K, Trauner M, et al.. Performance of non-invasive tests and histology for the prediction of clinical outcomes in patients with non-alcoholic fatty liver disease: an individual participant data meta-analysis. Lancet Gastroenterol Hepatol. 2023. PMID 37290471 · DOI
- Huang DQ, Noureddin N, Ajmera V, Amangurbanova M, Bettencourt R, Truong E, et al.. Type 2 diabetes, hepatic decompensation, and hepatocellular carcinoma in patients with non-alcoholic fatty liver disease: an individual participant-level data meta-analysis. Lancet Gastroenterol Hepatol. 2023. PMID 37419133 · DOI · PMC10812844
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-11-04; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-11-04.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.