Liraglutide Attenuates Hepatocyte Ferroptosis in an In Vitro Model of Metabolic Dysfunction-Associated Steatotic Liver Disease
- Design
- Cell / in-vitro · Biomarker outcome
- Match to healthy normal-weight adults aged 55–75
- Not human evidence[Auto] Non-human (animal or cellular) evidence; no direct inference to any human population.
- Could weight loss explain it?
- Unknown[Auto] Non-human study; weight-loss mediation not assessable.
- Study tier
- Study tier 4[Auto] Preclinical evidence; not clinical evidence for any human population.
- Assessment
- Version 1 · automatic, not yet reviewed by a person · Sep 13, 2026
Study facts come from the paper. Population match, weight-loss explanation and study tier are our judgments, made against the reference group of healthy normal-weight adults aged 55–75.
[Auto, unreviewed; last sentences of abstract] These effects were associated with modulation of ferroptosis-related gene expression, suggesting a mechanistic basis for the potential protective role of liraglutide in MASLD. Key words Ferroptosis " Free fatty acid " Liraglutide " Metabolic dysfunction-associated steatotic liver disease " Oxidative stress.
01Findings
What the study reported
- Drugs
- Liraglutide
- Comparator
- FFA
- Primary outcome
- Not extracted
- Effect
- Not extracted
- 95% confidence interval
- Not extracted
- Follow-up
- Not stated
- Adverse events
- Not extracted
- Limitations
- Auto-classified from abstract only; effect estimates, adverse events and limitations not extracted. Requires manual review.
Who was studied
- Baseline condition
- MASH / MASLD
Study quality details
- Study design
- Cellular / in-vitro
- Sample size
- not extracted
- Randomization
- no
- Blinding
- not stated
- Comparator
- not stated
- Follow up duration
- not stated
- Outcome type
- biomarker
- Replication
- not assessed (auto)
- Consistency with other evidence
- not assessed (auto)
- Population applicability
- VERY_INDIRECT
- Statistical precision
- not extracted
- Risk of bias
- not assessed (auto)
- Funding conflicts
- unclear
- Peer review status
- yes
02Funding
Funding and conflicts
- Funding
- not reported in abstract
- Industry funded
- Unclear
- Manufacturer
- None identified
- Sponsor role
- not reported in abstract
- Author conflicts
- not available in metadata
- Independent replication
- unknown
Funding is shown on every study and never used to score it.
04Source
The source, as retrieved
Abstract
This study examined the potential of liraglutide to attenuate ferroptosis in an in vitro model of metabolic dysfunction-associated steatotic liver disease (MASLD). HepG2 cells were allocated into three groups: control (Con), free fatty acid (FFA)-treated, and FFA with liraglutide treatment (FFA+LI). After 48 h of treatment, intracellular triglyceride (TG), glutathione (GSH), malondialdehyde (MDA), and iron levels were quantified using commercially available kits. Superoxide dismutase (SOD) activity was also measured. Lipid accumulation was visualized via Oil Red O staining. Expression of ferroptosis-associated genes was assessed through quantitative RT-PCR and western blotting. FFA treatment induced significant lipid accumulation, elevated TG, MDA, and iron levels, and reduced SOD activity and GSH levels compared to the Con group (all p<0.05). Additionally, FFA exposure increased the expression of TFR1 and downregulated SLC7A11, NRF2, and GPX4 (p<0.05 for all comparisons vs. Con). Liraglutide treatment partially reversed these changes, as evidenced by reduced MDA levels and iron content, downregulation of TFR1, and upregulation of NRF2 and GPX4 (FFA+LI vs. FFA, all p<0.05). Liraglutide demonstrated the ability to mitigate lipid accumulation, oxidative stress, and iron overload in HepG2 cells subjected to FFA-induced injury. These effects were associated with modulation of ferroptosis-related gene expression, suggesting a mechanistic basis for the potential protective role of liraglutide in MASLD. Key words Ferroptosis " Free fatty acid " Liraglutide " Metabolic dysfunction-associated steatotic liver disease " Oxidative stress.
Where this record came from
| Source | Retrieved | Identifier |
|---|---|---|
| pubmed | Sep 13, 2026 | 42695487 first ingestion |