Abstract

Diabetic cardiomyopathy (DCM) is one of the many complications of diabetes. DCM leads to cardiac insufficiency and myocardial remodeling and is the main cause of death in diabetic patients. Abnormal lipid metabolism plays an important role in the occurrence and development of DCM. Huangqi Shengmai Yin (HSY) has previously been shown to alleviate signs of heart disease. Here, we investigated whether HSY could improve cardiomyopathy caused by type 1 diabetes mellitus (T1DM) and improve abnormal lipid metabolism in the diabetic heart. Streptozotocin (STZ) was used to establish the T1DM mouse model, and T1DM mice were subsequently treated with HSY for eight weeks. The changes in the cardiac conduction system, histopathology, blood myocardial injury indices, and lipid content and expression of proteins related to lipid metabolism were evaluated. Our results showed that HSY could improve electrocardiogram; decrease the serum levels of CK-MB, LDH, and BNP; alleviate histopathological changes in cardiac tissue; and decrease myocardial lipid content in T1DM mice. These results indicate that HSY has a protective effect against T1DM-induced myocardial injury in mice and that this effect may be related to the improvement in myocardial lipid metabolism.

Highlights

  • Diabetes mellitus (DM) is a metabolic disease characterized by chronic hyperglycemia resulting from impaired insulin secretion and/or insulin resistance [1]

  • Effects of Huangqi Shengmai Yin (HSY) on Body Weight and Fasting Blood Glucose. e obvious characteristics of diabetes are a relative decrease in body weight gain and an increase in blood glucose

  • HSY treatment significantly decreased the levels of total cholesterol (TC), TG, lowdensity lipoprotein cholesterol (LDL), and Free fatty acid (FFA) and increased the level of high-density lipoprotein cholesterol (HDL) in comparison with the Diabetic cardiomyopathy (DCM) group. ere was no significant difference between the Control and

Read more

Summary

Introduction

Diabetes mellitus (DM) is a metabolic disease characterized by chronic hyperglycemia resulting from impaired insulin secretion and/or insulin resistance [1]. While several cellular processes play a role in the pathogenesis of DCM, including an imbalance in energy metabolism, oxidative stress, mitochondrial dysfunction, endoplasmic reticulum stress, impaired insulin signaling, myocardial fibrosis, and inflammation [5,6,7,8], a specific causative factor has not been identified. Excess utilization of FAs may cause impaired mitochondrial fatty acids oxidation (FAO), which further increases FAs accumulation [12, 13]. Is accumulation of FAs increases myocardial oxygen consumption and mitochondrial dysfunction, leading to cardiomyocyte death and ventricular dysfunction [14]. Erefore, addressing the abnormal metabolism of myocardial substrates by correcting the imbalance between the uptake and oxidation of FAs may be a potential method for the treatment of diabetic cardiomyopathy Excess utilization of FAs may cause impaired mitochondrial fatty acids oxidation (FAO), which further increases FAs accumulation [12, 13]. is accumulation of FAs increases myocardial oxygen consumption and mitochondrial dysfunction, leading to cardiomyocyte death and ventricular dysfunction [14]. erefore, addressing the abnormal metabolism of myocardial substrates by correcting the imbalance between the uptake and oxidation of FAs may be a potential method for the treatment of diabetic cardiomyopathy

Objectives
Methods
Results
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call