Antidiabetic Agents and Endothelial Dysfunction – Beyond Glucose Control

Diabetes is rapidly increasing worldwide, and the number of patients suffering from diabetes is projected to rise by 50% over the next 25 years, then affecting almost 600 million adults. Type 2 diabetes comprises 90–95% of all people with diabetes, and they constitute a patient group that carries a high burden of cardiovascular disease. The relationship between hyperglycaemia and macrovascular complications is still uncertain, at least in terms of the possibility of reducing cardiovascular events solely by improving glycaemic control. This MiniReview has thus focused on the effect of common antidiabetic agents, with emphasis on glucagon-like peptide-1, on the endothelial cells of the vasculature. Patients with type 2 diabetes suffer a two to four times higher risk of myocardial infarction and stroke than healthy persons. In addition to this, patients with diabetes have an increased atherosclerotic burden. Endothelial dysfunction is thought to be an early and important predictor of atherosclerosis and cardiovascular disease, and in people with type 2 diabetes, endothelial dysfunction is a common finding. It is therefore of importance to consider whether drugs used within the clinical management of Type 2 diabetes mellitus (T2DM) exert direct and positive effects on the vasculature independent of their glucose-lowering ability. This might serve to limit the adverse consequences of the macrovascular complications of T2DM, as dysfunction of endothelial cells is believed to contribute to a premature development of atherosclerosis.