Why the study?
Empagliflozin reduces heart failure risk, but the underlying mechanisms remain elusive; this study investigated its effect on branched-chain amino acid metabolism in diabetic cardiomyopathy.
Does empagliflozin improve cardiac structure and function in a mouse model of diabetic cardiomyopathy?
Population
Thirty male 8-week KK Cg-Ay/J diabetic mice and fifteen male 8-week C57BL/6J control mice
Comparison
Empagliflozin (3.75 mg/kg/day) vs diabetic model vs non-diabetic control
Design
Preclinical animal study
Follow-up
16 weeks
Key result
Empagliflozin significantly improved left ventricular ejection fraction and attenuated myocardial injury in diabetic mice by promoting branched-chain amino acid catabolism and inhibiting mTOR/p-ULK1 to enhance autophagy.
Authors
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Should not change clinical practice; hypothesis-generating for empagliflozin in diabetic cardiomyopathy.
Does empagliflozin improve cardiac structure and function in a mouse model of diabetic cardiomyopathy?
Absolute Event Rate: 52.2% vs 37.6%
p-value: p=0.005
Empagliflozin attenuates diabetic cardiomyopathy in mice by promoting branched-chain amino acid catabolism and enhancing autophagy via mTOR/p-ULK1 inhibition.
Zhang et al. (2023) studied Diabetic cardiomyopathy (n=45). Empagliflozin vs. No treatment was evaluated on Left ventricle ejection fraction (EF) (p=0.005). Empagliflozin significantly improved left ventricular ejection fraction and attenuated myocardial injury in diabetic mice by promoting branched-chain amino acid catabolism and inhibiting mTOR/p-ULK1 to enhance autophagy.