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When sotaglifozin was administered (30 mg/kg/d for 6 weeks) in obese rats, with metabolic-syndrome-related models of HF with HFpEF, and wild-type rats, this treatment ameliorated left atrial enlargement in HFpEF in vivo, prevented mitochondrial swelling, enhanced mitochondrial Ca 2+ buffer capacity in HFpEF, improved mitochondrial fission and reactive oxygen species (ROS) production during glucose starvation, and averted Ca 2+ accumulation upon glycolytic inhibition [122]
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