Presentation description

Obesity and type 2 diabetes are known risk factors for developing ventricular arrhythmias and are prevalent disorders that are increasing at an alarming rate with insufficient treatment options. Therefore, it is important to look at new cellular pathways that could provide unique and beneficial treatment options. Obesity and diabetes cause increased fat and lipid deposits as well as their building blocks, free fatty acids (FFAs). However, not much is known regarding how increased lipids (liptoxicity) can contribute to the development of ventricular arrhythmias. Therefore, we wanted to investigate the relationship between lipid metabolism and ventricular arrhythmias. One aspect of this relationship is leukotriene B4 (LTB4), a lipid mediator which has been shown to be increased in diabetes patients and can lead to ventricular arrhythmias in a high-fat diet guinea pig model. LTB4 can also lead to the increased production of FFAs, which have also been shown to contribute to arrhythmias. We hypothesized that due to increased LTB4, the lipid metabolic pathway is pathologically remodeled in lipotoxic hearts leading to ventricular arrhythmias. We tested this hypothesis by examining the expression of genes in the lipid metabolic pathway in lipotoxic hearts (induced by a high fat diet) compared to control hearts (represented by a low-fat diet). Changes in expression of these genes can suggest altered lipid synthesis, storage or breakdown, that could lead to arrhythmogenesis and therefore provide novel targets for future treatment options.