Advanced glycation end products (AGEs) are non-enzymatically formed in the body when lysine and arginine residues in proteins and peptides become irreversibly modified by reactive sugars such as glucose or carbonyls. AGEs can also be absorbed from dietary sources, in particular in westernised diets as a result of modern food processing or in cigarette smoke. Traditionally, AGEs have been investigated as contributors to diabetes complications since their production is facilitated by hyperglycaemia and the generation of reactive oxygen species. However, endogenously formed AGEs, haemoglobin A1c (HbA1c) and fructosamine albumin are used clinically everyday to track glucose control in people at risk for or already living with diabetes. There is also some evidence that AGE concentrations may serve as biomarkers for progressive injury at sites of diabetic complications and within the circulation. However, there has been a paradigm shift which suggests that AGEs may also have the ability to modulate insulin secretion, peripheral insulin sensitivity and immune cell function as well as cellular energetics and as such, may play a crucial role in the development of impaired glucose tolerance and diabetes per se. Many of these actions are postulated to be elicited by ligation to the receptor for advanced glycation end products, RAGE. This presentation will provide an overview of this area of research.