Obesity has become a prevalent pathology, especially in the developed world, being associated with the activation of numerous pathophysiologic mechanisms which may lead to cardiovascular diseases.

Our study aimed at assessing cardiac function in a rat model of heart failure and obesity.

Sprague-Dawley male rats (wild type, WT) and transgenic rats overexpressing β3-adrenergic receptors in endothelial cells (TGβ3) were either fed with standard diet (WT+SD, n=12; TGβ3+SD, n=12) or with hypercaloric diet (SD+HD, n=12; TGβ3+HD, n=12). For 35 weeks body-weight (BW), systolic blood pressure (SBP), echocardiographic structural and functional parameters were monitored. Oral glucose tolerance test (OGTT) was also performed.

HD induced an increase in BW in HD groups (∼10.08% for WT and ∼10.45% for TGβ3) since week 10 (W10), trend maintained until the end of the study. Regardless of WT or TGβ3 status, SBP (mmHg) was significantly increased by HD (∼12%), as measured at W35. Also, in the HD groups, hyperglycemia during OGTT was observed, suggesting insulinoresistance. Starting with W25, a decrease in early-to-late filing ratio (E/A ratio) in TGβ3+HD vs. TGβ3+SD was observed (0.97±0.04 vs. 1.11±0.07), while for WT+HD vs. WT+SD, reduction occurred at W35 (0.99±0.06 vs. 1.25±0.05). E’/A’ ratio followed the same trend, at W25: TGβ3+HD vs. TGβ3+SD (0.93±0.05 vs. 1.07±0.05), at W35: WT+HD vs. WT+SD (0.99±0.06 vs. 1.19±0.04). At W35, no significant change was registered in ejection fraction (%) between all groups (∼63%), suggesting no systolic dysfunction at this timepoint.

HD increased BW, SBP and glycemia. Alteration of diastolic function occurs at around W35 in obese WT rats, whereas in obese TGβ3 rats diastolic function alteration occurred earlier (W25).