Liraglutide causes large and rapid epicardial fat reduction

Objective Epicardial adipose tissue (EAT), the visceral fat depot of the heart, is a modifiable cardiovascular risk factor and emerging therapeutic target. Liraglutide, an analog of glucagon‐like peptide‐1, is indicated for the treatment of type 2 diabetes mellitus. Liraglutide has recently been shown to reduce cardiovascular risk. Nevertheless, whether liraglutide could reduce EAT is unknown. Methods To test the hypothesis, a 6‐month randomized, open‐label, controlled study was performed in 95 type 2 diabetic subjects with body mass index (BMI) ≥27 kg/m 2 and hemoglobinA1c ≤8% on metformin monotherapy. Individuals were randomized in two groups to receive additional liraglutide up to 1.8 mg s.c. once daily ( n = 54) or to remain on metformin up to 1,000 mg twice daily ( n = 41). Ultrasound‐measured EAT thickness was measured at baseline and at 3‐ and 6‐month follow‐ups. Results In the liraglutide group, EAT decreased from 9.6 ± 2 to 6.8 ± 1.5 and 6.2 ± 1.5 mm ( P < 0.001), accounting for a −29% and −36% of reduction at 3 and 6 months, respectively, whereas there was no EAT reduction in the metformin group; BMI and hemoglobinA1c improved only in the liraglutide group after 6 months. Conclusions Liraglutide causes a substantial and rapid EAT reduction. Liraglutide cardiometabolic effects may be EAT‐mediated.