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Using proteomic techniques the impact of the sodium-glucose transport protein 2 inhibitor empagliflozin on cardiac protein expression in a mouse model was assessed under normal and high-fat diet (HFD) conditions. We examined the effect of obesity on serological markers and heart function in obese mice treated with or without empagliflozin and used proteomic techniques to investigate alterations in cardiac protein expression. Using bioinformatic techniques, data were screened for differentially expressed proteins (DEPs) implicated in the putative mechanism of empagliflozin's cardioprotective effects. In C57BL/6 mice, HFD increased body weight, blood lipid, and glucose levels and was associated with structural damage to the heart. Empagliflozin reduces body weight, improves glucose and lipid metabolism, alleviates obesity-induced cardiac ventricular wall thickening, and lowers cardiac tissue collagen. The expression of several proteins was altered in the heart, mainly related to lipid metabolism. Following empagliflozin treatment, the expression of several lipid metabolism-related proteins was considerably reduced. Further examination of DEPs revealed that following empagliflozin treatment, the expressions of Apoe, Apoc1, Saa2, Apoa2, and Pon1 altered dramatically, suggesting that these proteins may be the main proteins that empagliflozin uses to treat obesity-induced aberrant lipid metabolism. Empagliflozin may protect the heart by altering the expression of genes including Apoe, Apoc1, Saa2, Apoa2, and Pon1, which are all involved in lipid metabolism disturbance in obesity. [ABSTRACT FROM AUTHOR]

Read the original articleNiu S, Ren Q, Chen S, et al. Diabetes Metab Syndr Obes. 2023;16:2549–2560.The authors have advised the correspondence section on page 2549 is incorrect. The correct correspondence details are as follows.Correspondence: Shuchun Chen, Department of Endocrinology, Hebei General Hospital, Shijiazhuang, Hebei, People's Republic of China, Email [email protected]The authors apologize for this error.By Shu Niu; Qingjuan Ren; Shuchun Chen; Xiaoyu Pan; Lin Yue; Xing Chen; Zelin Li and Ruoxi ZhenReported by Author; Author; Author; Author; Author; Author; Author; Author [Extracted from the article]