Journal
OBESITY
Volume 25, Issue 2, Pages 311-316Publisher
WILEY
DOI: 10.1002/oby.21718
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Funding
- Novo Nordisk
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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 229% and 236% 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.
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