New‐onset atrial fibrillation (NAF) is increased in the type 2 diabetic patient because of the presence of the metaboli syndrome and increased sympathetic activity. This results in inflammation, endothelial dysfunction and myocardial steatosis which, in turn, lead to atrial fibrosis and dilatation. The end result is the development of structural and electrical atrial remodeling. Drugs that lower insulin resistance, particularly pioglitazone, decrease the incidence of NAF while drugs that, through hypoglycaemia, stimulate the sympathetic nervous system, insulin and secretagogues, increase the incidence of NAF. Currently there is no evidence that GLP‐1 agonists, SGLT2 inhibitors and DPP‐4 inhibitors either accelerate or decelerate the development of NAF.