Adipocytokines modulate ionic currents – A key to lipotoxicity potentiated cardiac arrhythmia

Abstract

Obesity with excessive fat was an important risk factor for the occurrence or progression of cardiac arrhythmia. As compared to abdominal fat, the amount of epicardial fat more correlates with the occurrences of atrial fibrillation, which suggests the distinctive arrhythmogenic effects of epicardial fat. Adipose tissue secrets numerous adipocytokines, thus epicardial fat may have more cardiac effects than other body fat [1]. Adipocytokines can enhance local inflammation and generate myocardial remodeling, which play a role in the pathophysiology of arrhythmia. Fatty infiltration or fatty metamorphosis can induce abnormal automaticity from degenerated myocardial cells. Adipose tissues also serve as obstacles for an activation wave front or by producing atrial fibrosis, which may interfere with atrial conduction and enhance the generation of reentry circuits. Lee et al. investigated the effects of adipocytokines from different body fats on delayed rectifier K outward currents (IKr) in cardiomyocytes [2]. In their study, H9c2 cells were treated with adipocytokine-free medium (the Adipo-free group), and with adipocytokines from rat epicardial (central fat group) or limb (peripheral fat group) fat tissues. They found that adipocytokines significantly decreased IKr in H9c2 cells, and IKr was more prominently decreased by adipocytokines from epicardial fat than from limb fat. Although the mechanisms were not fully elucidated, Lee et al. pointed out the direct electrophysiological effects of adipocytokines and also demonstrated stronger ionic effects of epicardial fat than other body fat. Decreased IKr can prolong action