Since the discovery of the pancreatic islet hormone amylin in 1987, its metabolic effects have been investigated in a number of studies in animals and humans. Data from some early animal studies suggested that amylin might be associated with the development of insulin resistance, but other studies found that amylin had no effect on insulin sensitivity. More recently, studies performed using the human amylin analogue pramlintide in patients with Type 1 diabetes found that the hormone has no influence on either insulin-stimulated glucose uptake or the restraining effect of insulin on hepatic glucose production during periods of euglycaemia. Furthermore, during insulin-induced hypoglycaemia, pramlintide appears to increase the plasma concentrations of cortisol and growth hormone, and to stimulate the release of the gluconeogenic substrate lactate by the skeletal muscles. Taken together with evidence that, in short-term studies, pramlintide improved glycaemic control in patients with Type 1 diabetes who were also treated with insulin, these data suggest that pramlintide may have a role in the management of patients with diabetes. However, longer-term studies are required to ascertain whether these findings are sustained over time.