Heart matters: How glucose‐ and lipid‐modulating drugs remodel epicardial adipose tissue accumulation, inflammatory patterns and browning

Nov 27, 2025Diabetes, obesity & metabolism

How Blood Sugar and Fat-Lowering Drugs Change Fat Around the Heart, Inflammation, and Fat Burning

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Abstract

(EAT) may undergo pathological remodeling in cardiometabolic disorders, leading to increased thickness and inflammation.

EAT plays a crucial role in supporting heart energy metabolism and thermoregulation under normal conditions.
In conditions like obesity and heart failure, EAT experiences changes such as increased thickness and immune cell infiltration.
These pathological changes in EAT are associated with myocardial fibrosis and coronary atherosclerosis.
Pharmacological agents can modulate EAT and may reduce its thickness while enhancing insulin sensitivity.
Sodium-glucose cotransporter 2 inhibitors and glucagon-like peptide-1 receptor agonists are noted for their consistent effects on EAT, promoting a less inflammatory and more active metabolic state.

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(EAT) is a metabolically active visceral fat depot located between the myocardium and the visceral pericardium, exerting direct paracrine and vasocrine effects on the heart and coronary vessels. Under physiological conditions, EAT supports myocardial energy metabolism and thermoregulation through fatty acid supply and adaptive metabolic flexibility. In cardiometabolic disorders such as obesity, type 2 diabetes, and heart failure, EAT undergoes pathological remodelling characterized by increased thickness, adipocyte hypertrophy, immune cell infiltration, and secretion of pro-inflammatory and fibrotic mediators. These alterations contribute to myocardial fibrosis, stiffness, and coronary atherosclerosis, particularly in heart failure with preserved ejection fraction. Pharmacological modulation of EAT has therefore emerged as a promising therapeutic approach in cardiovascular prevention. Agents such as statins, peroxisome proliferator-activated receptor gamma agonists, adenosine monophosphate-activated protein kinase activators, glucagon-like peptide-1 receptor agonists, and sodium-glucose cotransporter 2 inhibitors exert both systemic and depot-specific effects. They reduce EAT thickness, suppress inflammatory signalling, enhance insulin sensitivity, and promote adipocyte browning and oxidative metabolism. Among these, sodium-glucose cotransporter 2 inhibitors and glucagon-like peptide-1 receptor agonists show the most consistent effects in shifting EAT towards a less inflammatory and more metabolically active phenotype. The goal of this review is to provide an overview of current pharmacological interventions that influence EAT and to summarize how much is known about their molecular mechanisms from in vitro and in vivo studies. The target audience includes cardiovascular researchers and clinicians seeking to better understand how metabolic and antidiabetic therapies modulate cardiac fat biology and function.

Key numbers

20%

Reduction in volume

Observed with semaglutide in patients with type 2 diabetes and obesity.

9% decrease in volume

Measured in type 2 diabetes patients over 24 weeks.

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Heart matters: How glucose‐ and lipid‐modulating drugs remodel epicardial adipose tissue accumulation, inflammatory patterns and browning

Abstract

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