Liraglutide Ameliorates Atrial Fibrillation in Association with Enhanced Adiponectin Signaling in Epicardial Adipose Tissue
- Design
- Animal study · 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 20, 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; quoted from abstract conclusions] Liraglutide alleviates AF by increasing ADPN secretion and AdipoR1 expression in the EAT, improving local lipid metabolism, and attenuating inflammation. These findings establish a correlational association between liraglutide treatment, favorable modulation of the EAT phenotype, and AF amelioration, and propose a testable hypothesis that adiponectin signaling is involved in liraglutide-mediated cardioprotection.
01Findings
What the study reported
- Drugs
- Liraglutide
- 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
- Obesity status
- obesity/overweight present (all or most)
Study quality details
- Study design
- Preclinical (animal)
- 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
- Medical Science Research Project of Hebei
- Industry funded
- Unclear
- Manufacturer
- None identified
- Sponsor role
- not reported in abstract
- Author conflicts
- Declarations. Ethics: The animal study protocol was approved by the Ethics Committee of Hebei Provincial People’s Hospital [2025-DW-142]. All experiments were conducted in strict accordance with the National Research Council’s Guide for the Care and Use of Laboratory Animals and reported following the ARRIVE guidelines. Competing interests: The authors declare no competing interests. Generative AI: No generative AI or AI-assisted technolog were used in the development of this manuscript. The authors assume full responsibility for all content.
- Independent replication
- unknown
Funding is shown on every study and never used to score it.
04Source
The source, as retrieved
Abstract
[PURPOSE] Atrial fibrillation (AF) is associated with obesity and epicardial adipose tissue (EAT) dysfunction. Although glucagon-like peptide-1 receptor agonists (GLP-1 RAs), such as liraglutide, exert cardiovascular benefits, the underlying mechanisms, particularly those related to EAT and adipokine signaling remain unclear. [METHODS] AF rat model was established using acetylcholine-CaCl₂ infusion. Model rats were treated with liraglutide or saline, and cardiac functions were assessed using electrocardiography (ECG) and echocardiography. Myocardial and EAT morphology was examined histologically. The levels of adiponectin (ADPN), inflammatory factors, and lipids were measured using enzyme-linked immunosorbent assay, and the protein levels of ADPN and its receptor were evaluated through western blotting. In vitro, 3T3-L1 adipocytes were treated with TNF-α to simulate a model of dysregulated lipid metabolism and inflammation. Subsequently, HL-1 cells were treated with the conditioned medium from 3T3-L1 cells. The interaction between adipocytes and cardiomyocytes was evaluated by assessing HL-1 cell proliferation, apoptosis, and levels of ADPN and inflammatory factors. [RESULTS] Liraglutide significantly reduced the duration of AF, improved cardiac function (decreased E/E', increased ejection fraction and LAACF), ameliorated myocardial fibrosis, and restored EAT morphology. Mechanistically, liraglutide specifically enhanced ADPN secretion and upregulated AdipoR1 expression in EAT, reduced interleukin (IL)-6 and IL-1β levels, and decreased free fatty acid (FFA) and triglyceride content. Notably, using an ADPN-neutralizing antibody in vitro, we demonstrated that ADPN mediates the protective effects of liraglutide on cardiomyocytes, suggesting the role of EAT-derived ADPN signaling. [CONCLUSION] Liraglutide alleviates AF by increasing ADPN secretion and AdipoR1 expression in the EAT, improving local lipid metabolism, and attenuating inflammation. These findings establish a correlational association between liraglutide treatment, favorable modulation of the EAT phenotype, and AF amelioration, and propose a testable hypothesis that adiponectin signaling is involved in liraglutide-mediated cardioprotection.