Abstract
Obesity has been demonstrated to be linked to atrial fibrillation (AF) with atrial enlargement and tissue fibrosis. Long-term high calorie intake is the main reason for the prevalence of obesity. To investigate the possible causes of AF, such as chronic high-fat diet (HFD), and to identify the underlying mechanisms, the present study analyzed a variety of structural and gap junctional electrophysiological alterations in the atria of female rats fed an HFD. After consistent HFD feeding of female rats for 12 weeks, hematoxylin and eosin (H&E) and Masson's staining, RT-qPCR, western blotting, immunofluorescence and TUNEL staining were performed. In our study, approximately 3/5 of the HFD-fed rats (HFD-OB, n=13) displayed a significant increase in body weight, while the other 2/5 did not (HFD-NOB, n=8). In addition, the atrial weight of the HFD-OB and HFD-NOB rats was markedly heavier, as compared to the rats fed a normal diet (CT, n=20). According to the plasma lipid levels, both HFD-OB and HFD-NOB rats exhibited dyslipidemia. Furthermore, H&E staining revealed broadened interstitial space and myocyte disarray in atria of the HFD-fed rats (i.e., HFD-OB and HFD-NOB rats). Expression levels of atrial fibrosis relevant factors, trans...Continue Reading
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