Exercise Training Restores Cardiac MicroRNA-1 and MicroRNA-29c to Nonpathological Levels in Obese Rats

André C Silveira,Carlos Eduardo Negrão,João L P Gomes,Glória G F Mota,Edilamar M Oliveira,Úrsula P R Soci,Diego L Barretti,Tiago Fernandes

doi:10.1155/2017/1549014

André C Silveira, Carlos Eduardo Negrão + Show 6 more

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https://doi.org/10.1155/2017/1549014

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Abstract

We previously reported that aerobic exercise training (AET) consisted of 10 weeks of 60-min swimming sessions, and 5 days/week AET counteracts CH in obesity. Here, we evaluated the role of microRNAs and their target genes that are involved in heart collagen deposition and calcium signaling, as well as the cardiac remodeling induced by AET in obese Zucker rats. Among the four experimental Zucker groups: control lean rats (LZR), control obese rats (OZR), trained lean rats (LZR + TR), and trained obese rats (OZR + TR), heart weight was greater in the OZR than in the LZR group due to increased cardiac intramuscular fat and collagen. AET seems to exert a protective role in normalizing the heart weight in the OZR + TR group. Cardiac microRNA-29c expression was decreased in OZR compared with the LZR group, paralleled by an increase in the collagen volumetric fraction (CVF). MicroRNA-1 expression was upregulated while the expression of its target gene NCX1 was decreased in OZR compared with the LZR group. Interestingly, AET restored cardiac microRNA-1 to nonpathological levels in the OZR-TR group. Our findings suggest that AET could be used as a nonpharmacological therapy for the reversal of pathological cardiac remodeling and cardiac dysfunction in obesity.

Highlights

Obesity results from a combination of excessive food energy intake, lack of physical activity, and genetic susceptibility [1,2,3,4]
The aerobic exercise training (AET) normalized epididymal fat content in the obese Zucker rats (OZR) + TR (0.04 ± 0.003 g/mm) groups compared with the control (0.126 ± 0.012 g/mm) and trained (0.022 ± 0.012 g/mm) lean Zucker rats (LZR) groups (Figure 1(b))
A previous study from our group showed pathological cardiac hypertrophy (CH) in OZR observed by echocardiography and LV mass/tibial length (TL) ratio [1]. Corroborating these data, we showed that the HW/TL ratio was increased 29% in the OZR group compared with the LZR group, Swimming

Summary

Introduction

Obesity results from a combination of excessive food energy intake, lack of physical activity, and genetic susceptibility [1,2,3,4]. Obesity induces systemic inflammation and contributes to the development of atherosclerosis and cardiovascular diseases, which cooperate with the pathological cardiac hypertrophy (CH) phenotype [6, 7]. Cardiac remodeling induced by obesity is a compensatory adaptation to volume overload and/or continuous pressure imposed on the heart [8]. Studies in obese Zucker rats show an increase in left ventricular mass accompanied by pathological CH molecular markers such as β-myosin heavy chain (β-MHC), atrial natriuretic factor (ANF), α-skeletal actin; cardiac dysfunction; and heart failure [8,9,10]. The diastolic dysfunction in obesity is induced both by increased collagen content and by damage to calcium signaling pathways mediated by proteins of intracellular calcium removal, such as SERCA-2a and the sodium/calcium exchanger NCX1 [11, 12]

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