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Cardiometabolic Modulation by Semaglutide Contributes to Cardioprotection in Rats with Myocardial Infarction
Haihao Yan1,2, Wenjing Yao2, Yanhong Li1
1Department of Internal Medicine, Graduate School of Hebei Medical University, Shijiazhuang, Hebei, 050017, People's Republic of China.
Insights
Semaglutide treatment improved cardiac function and reduced fibrosis in rats after myocardial infarction. It also modulated glucose, lipid, and organic acid metabolism, suggesting therapeutic potential for heart attack recovery.
Area of Science:
- Cardiology
- Metabolomics
- Pharmacology
Background:
- Acute myocardial infarction (AMI) poses a significant clinical challenge.
- Semaglutide shows potential in cardiovascular disease, but its role in AMI requires further investigation.
Purpose of the Study:
- To investigate the effects and mechanisms of semaglutide in a rat model of acute myocardial infarction.
- To analyze the impact of semaglutide on cardiac function, cardiac fibrosis, and metabolic profiles post-MI.
Main Methods:
- Twenty-four male Sprague-Dawley rats were divided into control, MI, and semaglutide-treated groups.
- Evaluated cardiac function via echocardiography, cardiac fibrosis via histopathology, and metabolic profiles using untargeted LC-MS/MS metabolomics.
Main Results:
- Semaglutide treatment improved left ventricular ejection fraction and reduced myocardial collagen volume fraction.
- Metabolomic analysis revealed significant alterations in benzenoid, lipid, and organic acid metabolism pathways.
- Key metabolites involved in metabolic reprogramming were identified, including Docusate sodium, Choline sulfate, and Lactosamine.
Conclusions:
- Semaglutide significantly ameliorated myocardial fibrosis and metabolic dysregulation in rats post-MI.
- The mechanism involves modulating glucose, lipid, and organic acid metabolism.
- Specific targeted metabolites are implicated in the metabolic reprogramming induced by semaglutide.
Background:
Acute myocardial infarction (AMI) is a significant clinical challenge. Semaglutide has therapeutic potential in cardiovascular disease management, but its specific impact and mechanisms in AMI are not fully understood.
Methods:
Twenty-four male Sprague-Dawley rats were divided into three groups: control (Control), infarction-only (MI), and semaglutide-treated (SEMA). Weight, blood glucose, and lipid profiles were analyzed. Cardiac function was evaluated via echocardiography. Histopathological assessment and immunohistochemical analysis were performed. Untargeted metabolomic analysis using LC-MS/MS was utilized.
Results:
Semaglutide treatment was associated with a reduction in body weight, blood glucose, total cholesterol (TC), and low-density lipoprotein cholesterol (LDL-C), as well as an enhancement in the left ventricular ejection fraction (Control vs MI vs SEMA, 69.13±4.30 vs 30.16±3.17 vs 39.81±6.13, P < 0.05). It also had a lower collagen volume fraction (3.05 vs 34.05 vs 17.73, P < 0.05) and ameliorated the accumulation of glycogen in the myocardium. Metabolomic profiling revealed differentially expressed metabolites between the control/MI and MI/SEMA groups, predominantly within benzenoid, lipid, and organic acid categories. Pathway enrichment analysis highlighted amino sugar and nucleotide sugar metabolism, chlorocyclohexane and chlorobenzene degradation, and phenylalanine, tyrosine, and tryptophan biosynthesis. Random forest analysis identified key metabolites, including downregulated Docusate sodium, 1-(2-Thienyl)-1-heptanone, and Adenylyl-molybdopterin, alongside upregulated Methylenediphosphonic acid, Choline sulfate, and Lactosamine.
Conclusion:
Semaglutide significantly ameliorated myocardial fibrosis and metabolic dysregulation in rats post-myocardial infarction. Its mechanism involves modulating glucose metabolism, lipid metabolism, and organic acid metabolism. Targeted metabolites, including Docusate sodium, 1-(2-Thienyl)-1-heptanone, Adenylyl-molybdopterin, Methylenediphosphonic acid, Choline sulfate, and Lactosamine, are implicated in the metabolic reprogramming induced by semaglutide.
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