Melatonin administration increased susceptibility to atrial fibrillation in obese mice, likely due to increased lipid stress and impaired atrial Akt signaling.
Does melatonin increase susceptibility to atrial fibrillation in a mouse model of obesity?
Melatonin supplementation in obese mice increases susceptibility to atrial fibrillation by impairing atrial Akt signaling due to increased lipid stress, suggesting caution for its use in obese patients.
Melatonin has been proven to have antiarrhythmic potential; however, several studies have recently challenged this view. Herein, using a mouse model of obesity-induced atrial fibrillation (AF), we tentatively explored whether exogenous melatonin supplementation could increase AF susceptibility in the context of obesity. We observed that an 8-week drinking administration of melatonin (60 µg/ml in water) induced a greater susceptibility to AF in obese mice, although obesity-induced structural remodeling was alleviated. An investigation of systemic insulin sensitivity showed that melatonin treatment improved insulin sensitivity in obese mice, whereas it inhibited glucose-stimulated insulin secretion. Notably, melatonin treatment inhibited protein kinase B (Akt) signaling in the atria of obese mice and palmitate-treated neonatal rat cardiomyocytes, thereby providing an AF substrate. Melatonin increased lipid stress in obesity, as evidenced by elevated lipid accumulation and lipolysis-related gene expression, thus contributing to the impairment in atrial Akt signaling. Taken together, our results demonstrated that melatonin could increase AF susceptibility in obesity, probably due to increased lipid stress and resultant impairment of atrial Akt signaling. Our findings suggest that special precautions should be taken when administering melatonin to obese subjects.
Qin et al. (Sat,) conducted a other in Obesity-induced atrial fibrillation. Melatonin was evaluated on Susceptibility to atrial fibrillation. Melatonin administration increased susceptibility to atrial fibrillation in obese mice, likely due to increased lipid stress and impaired atrial Akt signaling.