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“We reported EAT density changed from −92.4 to −87.5 HU on semaglutide, and the EAT mean density increased with treatment by 4.9 HU (P < 0.010). Multiple groups, including our own, have published widely that increased density is consistent with better outcomes and less diabetes, metabolic syndrome, and heart failure... Quantification of EAT density represents the quality of fat as it reflects the complex interplay between brown and white fat, inflammation and fibrosis of the EAT”
“This work makes an important contribution to understanding how metabolic interventions like the GLP-1-RA semaglutide can impact EAT ectopic fat depot and its associated proinflammatory pathways, which are thought to influence myocardial function. This study might suggest semaglutide as a preventive therapeutic strategy for reducing inflamed epicardial fat genesis. These findings have the potential to inform future clinical strategies focused on reducing inflammation in fat depots as a way to mitigate cardiovascular disease, particularly in the context of metabolic disorders like obesity and type 2 diabetes.”
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Manubolu et al. (2024) studied this question.
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