Résumé
Atrial fibrillation (AF) is the most prevalent cardiac arrhythmia, and its global incidence is increasing worldwide. Major risk factors for AF encompass body mass index, hypertension, diabetes mellitus, advanced age and various circulating biomarkers. Notably, these multiple risk factors can be “programmed” by nutritional disturbances during both the fetal and post-natal periods.
Our aim was to assess the impact of post-natal overfeeding (PNOF) on body weight evolution, glucose metabolism, cardiac function and the occurrence of spontaneous or stimulated AF episodes in adult male mice.
PNOF was induced by reducing the litter size of C57/BL6 mice 2 days after birth: normally-fed group (NF) was composed of 9 male pups/mother and overfed group (OF) of 3 pups/mother. Glycemic tests were realized after 6hours fasting and echocardiography was performed using VEVO 770. Electrocardiograms (ECG) were monitored by telemetry with a signal transmitter-receiver connected to a data acquisition system. Electrophysiological studies were conducted via closed chest transesophageal approach on gaseous anaesthetized mice: AF episodes were measured spontaneously or induced through transesophageal atrial stimulations.
PNOF induced an early and sustained increase in body weight in the OF group, starting from weaning (+23%) and persisting until 6 months of age (+23%). PNOF mice presented glucose metabolism imbalance, especially insulin resistance. Echocardiographic measurements revealed an impairment of contractile function, indicated by a decrease in left ventricular ejection fraction (–11%). Finally, PNOF mice exhibited a higher occurrence of both spontaneous and stimulated AF episodes: none of the control group mice experienced any AF episodes, while 30% of PNOF mice displayed AF events in both contexts.
Short-term PNOF induced early and long-lasting alterations in body weight, glucose metabolism and cardiac contractility. Moreover, mice submitted to PNOF exhibited an increased occurrence of AF episodes, both spontaneously and in response to transesophageal atria activation. These electrophysiological changes may be linked to complex histological and biochemical remodeling, potentially involving a decrease in brain-derived neurotropic factor (BDNF).