INS and atrial fibrillation: Atrial lipo-toxicity elicits mitochondrial and endoplasmic reticulum dysfunctions, activates apoptotic cell death signaling, and interferes with insulin-stimulated glycogen uptake, which together engage mechanisms underlying alterations in the atrial anatomy (hypertrophy and fibrosis [114]) and electrophysiology (connexin 43 lateralization, conduction propagation impairment [115]), culminating in AF.