Abstract
BackgroundDiabetes mellitus is an important risk factor for atrial fibrillation (AF) development. Sodium–glucose co-transporter-2 (SGLT-2) inhibitors are used for the treatment of type 2 diabetes mellitus (T2DM). Their cardioprotective effects have been reported but whether they prevent AF in T2DM patients are less well-explored. We tested the hypothesis that the SGLT-2 inhibitor, empagliflozin, can prevent atrial remodeling in a diabetic rat model.MethodsHigh-fat diet and low-dose streptozotocin (STZ) treatment were used to induce T2DM. A total of 96 rats were randomized into the following four groups: (i) control (ii) T2DM, (iii) low-dose empagliflozin (10 mg/kg/day)/T2DM; and (iv) high-dose empagliflozin (30 mg/kg/day)/T2DM by the intragastric route for 8 weeks.ResultsCompared with the control group, left atrial diameter, interstitial fibrosis and the incidence of AF inducibility were significantly increased in the DM group. Moreover, atrial mitochondrial respiratory function, mitochondrial membrane potential, and mitochondrial biogenesis were impaired. Empagliflozin treatment significantly prevented the development of these abnormalities in DM rats, likely via the peroxisome proliferator-activated receptor-c coactivator 1α (PGC-1α)/nuclear respiratory factor-1 (NRF-1)/mitochondrial transcription factor A (Tfam) signaling pathway.ConclusionsEmpagliflozin can ameliorate atrial structural and electrical remodeling as well as improve mitochondrial function and mitochondrial biogenesis in T2DM, hence may be potentially used in the prevention of T2DM-related atrial fibrillation.
Highlights
Atrial fibrillation (AF) is the commonest type of sustained cardiac arrhythmia with an age-related increaseRecently there have been numerous trial and real-world studies on the cardiovascular benefits of sodium–glucose co-transporter-2 (SGLT-2) inhibitors in type 2 diabetic patients
We investigated the effects of empagliflozin (EMPA), a commercially available and highly selective Sodium–glucose co-transporter-2 (SGLT-2) inhibitor, on atrial remodeling in high-fat diet (HFD)/streptozotocin (STZ)-induced diabetic rats
In the high-dose empagliflozin group, LAD, interventricular septal thickness (IVST), and left ventricular posterior wall thickness (LVPWT) were significantly decreased compared with the Diabetes mellitus (DM) group (p < 0.05), whilst no significant difference was observed after low-dose empagliflozin treatment (p > 0.05)
Summary
There have been numerous trial and real-world studies on the cardiovascular benefits of sodium–glucose co-transporter-2 (SGLT-2) inhibitors in type 2 diabetic patients. We investigated the effects of empagliflozin (EMPA), a commercially available and highly selective SGLT-2 inhibitor, on atrial remodeling in high-fat diet (HFD)/streptozotocin (STZ)-induced diabetic rats. Sodium–glucose co-transporter-2 (SGLT-2) inhibitors are used for the treatment of type 2 diabetes mellitus (T2DM). Their cardioprotective effects have been reported but whether they prevent AF in T2DM patients are less well-explored. We tested the hypothesis that the SGLT-2 inhibitor, empagliflozin, can prevent atrial remodeling in a diabetic rat model
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