Frontiers in Bioscience-Scholar (FBS) is published by IMR Press from Volume 13 Issue 1 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.
Diabetes, obesity and increased body mass index are associated with changes in metabolism that lead to an inadequate reservoir or use of ATP in the heart and susceptibility to arrhythmia. Lack of availability of ATP and abnormal levels of metabolic end products can cause gene reprogramming and electrical remodelling that make myfibers susceptible to arrhythmia. Understanding the metabolic aberrations that lead to arrhythmia require better understanding of cardiac metabolism. Here, I discuss metabolic genes, enzymes and reducing equivalents and functional aspects of metabolic-induced arrhythmia with a special focus on atrial induced arrhythmia. It appears that normalisation of altered Kv1.5 channel, an oxygen sensing ion channel and fulfillment of oxygen demand by myocardium might offer a new strategy for preventing alterations of repolarisation that cause arrhythmia.