Empagliflozin alters lipid metabolism in the myocardium and liver in a prediabetes model with severe dyslipidemia

• DOI: 10.3389/fphar.2024.1393946
• Publication Date: 2024-07-04T04:55:17Z
• Authors: Denisa Miklankova; Irena Markova; Martina Hüttl; Hana Malinska
• Keywords: Empagliflozin; Dyslipidemia; Lipotoxicity

Background and aims Recent studies suggest that empagliflozin reduces total cardiovascular mortality in both diabetic nondiabetic subjects. Although the exact mechanism is unclear, it understood to positively affect myocardial energetics, including metabolism of ketone bodies, lipids, fatty acids. In this study, we compared effects on lipid heart liver a prediabetic rat model with severe dyslipidemia. Materials methods Wistar rats served as control group, while hereditary hypertriglyceridemic (HHTg) were used nonobese, model. Rats treated or without at dose 10 mg/kg body weight (BW) for 8 weeks. Results HHTg rats, decreased adiposity, improved glucose tolerance, serum triacylglycerols (TAGs) ( p < 0.001). Empagliflozin activity gene expression lipogenic enzyme SCD-1 0.001) myocardium, which may have led decrease ectopic accumulation TAGs lipotoxic diacylglycerols lysophosphatidylcholines Changes phosphatidylcholine/phosphatidylethanolamine ratio 0.01) acid profile phospholipids contributed antifibrotic empagliflozin. The anti-inflammatory evidenced by an increased IL-10/TNFα 0.001), marked arachidonic metabolites (20-HETE, increase PUFA (14,15-EETs, myocardium. However, did not significantly either concentration utilization bodies. liver, lipogenesis intermediates. Its effect alterations n-3 was less pronounced than Conclusion Our findings treatment reduced neutral lipids intermediates altered PUFA. heart, metabolism, likely associated drug. We assume these contribute cardioprotective states