Abstract
Aim: Adropin (ADR) is a novel regulatory polypeptide and has important effects on energy metabolism in the heart. However, it is still unclear whether ADR can relieve ventricular remodeling in DCM. Therefore, this study was conducted to assess the effect of ADR on myocardial fibrosis in DCM rats.Materials and Methods: Twenty Wistar rats were randomly assigned into four groups: healthy control group (CON), DCM model group (DCM), DCM model treated with ADR group (ADR) and DCM model treated with perindopril group (PER). Collagen volume fraction (CVF) and perivascular collagen area (PVCA) were calculated. Diastolic function was assessed by echocardiography. The mitochondrial membrane potential assay was conducted by Rhodamine 123 staining. The protein expression levels of Col I, Col III, Mitofusin-1, Mitofusin-2 and Drp1 were evaluated using western blot.Results: Compared to CON group, CVF, PVCA and the relative protein expression of Col I, Col III and Drp1 increased in DCM group. And the relative expression of Mitofusin-1 and Mitofusin-2 proteins decreased. During our investigations, CVF, PVCA and the relative protein expression of Col I, Col III and Drp1 decreased in ADR treated rats compared to DCM group. The diastolic function was elevated in ADR group. The fluorescence of Rhodamine 123 and the expression of Mitofusin-1 and Mitofusin-2 also increased in ADR group.Conclusion: Our study demonstrated that ADR could alleviate myocardial fibrosis and improve diastolic function in DCM rats. ADR may be a putative candidate for the treatment of DCM.
Highlights
Diabetic cardiomyopathy (DCM) is a type of cardiovascular damage and recognized as a specific entity in patients with type 2 diabetes mellitus, excluding coronary atherosclerotic heart disease, hypertrophic cardiomyopathy, hypertensive heart disease and other heart diseases [1, 2]
The rats were randomly assigned into four groups: healthy control group (CON), DCM model group (DCM), DCM model treated with ADR group (ADR) and DCM model treated with perindopril group (PER)
We found that ADR reduced LVW/BW ratio, E/A ratio, Strain rate in early (SRe)/SRa ratio, CVF, PVCA and the relative expression of Col I and Col III proteins, indicating that ADR can alleviate myocardial fibrosis and improve diastolic function in DCM rats
Summary
Diabetic cardiomyopathy (DCM) is a type of cardiovascular damage and recognized as a specific entity in patients with type 2 diabetes mellitus, excluding coronary atherosclerotic heart disease, hypertrophic cardiomyopathy, hypertensive heart disease and other heart diseases [1, 2]. Myocardial fibrosis, small vessel disease and autonomic dysfunction are associated with the development of DCM. The number of deaths caused by diabetes mellitus and its complications is as high as 1.5 to 5 million each year. More than half of diabetes mellitus related fatal or disabling events are caused by DCM [3]. Mitochondria play a pivotal role in cellular energy transduction. One-third of the heart’s volume is composed of mitochondria alone as they are essential organelles in the production of adenosine triphosphate from the oxidation of fatty acid and glucose [4]. Mitochondrial dysfunction may contribute to the development of DCM by inducing insulin resistance in skeletal muscle, adipose tissue and pancreatic β-cells [5]
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