The study looks at the fat around the heart (epicardial fat) and how it gets inflamed, which can worsen heart disease. It shows that the heart fat has receptors for GLP‑1 and GIP drugs like semaglutide, meaning these drugs can directly affect this fat. Triggering those receptors might help the fat remodel in a healthier way, potentially lowering heart risk, but the idea is still being explored.

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. 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. Cardiovascular effects of liraglutide, semaglutide and tirzepatide can be mediated by EAT inflammation.