There is substantial evidence supporting the fact that ectopic fat accumulation is an important contributor to type 2 diabetes complications and cardiovascular risk [1]. Epicardial adipose tissue (EAT), located between the myocardium and the visceral layer of the pericardium has been associated with atrial fibrillation and with coronary artery disease [2, 3] and its abundance predicts the number of cardiac events within 8 years [4]. In addition, myocardial steatosis has been shown to be an independent predictor of diastolic dysfunction [5] [6]. Furthermore, in type 2 diabetic patients, bariatric surgery can reduce cardiac ectopic fat accumulation and improve cardiac function [7] [8]. When added to standard care, 10 or 25 mg/d of empagliflozin, an inhibitor of sodium-glucose cotransporter 2 (iSGLT2), significantly reduces the risk of death, cardiovascular death, and hospitalisation for heart failure among individuals with type 2 diabetes and established cardiovascular disease when compared to placebo [9]. The mechanisms of empagliflozin-improved cardiovascular outcomes in type 2 diabetic patients at high risk of cardiovascular events are not known. We hypotheses that empaglifozin could modulate cardiac ectopic fat and cardiac metabolism in obese type 2 diabetic patients.

Inclusion Criteria:

• Age > 18 years,
• Type 2 diabetes based on the disease diagnostic criteria as described by the WHO,
• HbA1c > 7% and < 10 %
• Stable glucose-lowering therapy for at least 3 weeks before randomization
• Estimated glomerular filtration rate > 60/ml (MDRD)
• Signed informed consent form obtained prior to any study procedure

Exclusion Criteria:

• Evolutive or planned pregnancy during the six months
• Lactation
• Recent weight loss (>5% of body weight within one month),
• Treatment modifying adipose distribution such as corticoids
• Acute coronary syndrome or instable angina during the last 2 months,
• MRI contraindication (metal cardiac valve, pace maker, metal foreign body, claustrophobia)