Epicardial Fat Inflammation and GLP-1/GIP Receptor Analogs: Are we Shifting our Perspective?
- 01-12-2025
- Semaglutide
- Pericardial Disease (AL Klein and CL Jellis, Section Editors)
- Author
- Gianluca Iacobellis
- Published in
- Current Cardiology Reports | Issue 1/2025
Abstract
Purpose of the Review
Epicardial adipose tissue (EAT), the visceral fat of the heart, is highly inflammatory fat depot with pro-inflammatory transcriptome and proteosome. EAT contributes to the development and progression of coronary artery disease (CAD) and atrial fibrillation (AF) through multifactorial inflammatory pathways. However, the paradigm linking EAT inflammation and cardiovascular risk was recently reevaluated.
Recent Findings
EAT inflammation may be also necessary process for adipose tissue remodeling and expansion to accommodate excess lipids. EAT inflammation may be also considered an adaptive response of adipose tissue to the effects of glucagon-like peptide-1 receptor (GLP-1Rs) and glucose-dependent insulinotropic polypeptide (GIP) analogs. The presence of GLP-1 (GLP-1R) and GIP receptors (GIP-R) suggest direct interaction of these agents with EAT. EAT GLP-1R and GIP-R activation can induce a beneficial balance between increased adipogenesis and reduced ectopic fat accumulation.
Summary
Cardiovascular effects of liraglutide, semaglutide and tirzepatide can be mediated by EAT inflammation.
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- Title
- Epicardial Fat Inflammation and GLP-1/GIP Receptor Analogs: Are we Shifting our Perspective?
- Author
-
Gianluca Iacobellis
- Publication date
- 01-12-2025
- Publisher
- Springer US
- Keywords
-
Semaglutide
Tirzepatide
Liraglutide
GLP-1 Receptor Agonists
GLP-1 Receptor Agonists
Atrial Fibrillation - Published in
-
Current Cardiology Reports / Issue 1/2025
Print ISSN: 1523-3782
Electronic ISSN: 1534-3170 - DOI
- https://doi.org/10.1007/s11886-025-02325-5
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