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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)
Published in:

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.
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
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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  • Bayer HealthCare Pharmaceuticals Inc.
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Abstract graphic of layered, concentric circular shapes in bright green, pink, blue, and purple on a dark blue background. The rings and segments form a complex radial pattern without text/© Springer Health+ IME