Diabetes frequently occurs during corticosteroid treatment, sometimes necessitating urgent therapeutic management, with insulin for example. Corticosteroids induce insulin resistance in the liver, adipocytes and skeletal muscle, and have direct deleterious effects on insulin secretion. The development of insulin resistance during corticosteroid treatment, and the insufficient adaptation of insulin secretion, are key elements in the pathophysiology of corticosteroid-induced diabetes. The capacity of pancreatic β-cells to increase insulin secretion in response to insulin resistance is partly genetically determined. A familial history of type 2 diabetes is, therefore, a major risk factor for diabetes development on corticosteroid treatment. Corticosteroid treatments are usually initiated at a fairly high dose, which is subsequently decreased to the lowest level sufficient to achieve disease control. Pharmacological management of diabetes is needed in patients with blood glucose levels exceeding 2.16 g/l (12 mmol/l) and insulin therapy can be started when blood glucose levels are higher than 3.6 g/l (20 mmol/l) with clinical symptoms of diabetes. Insulin can then be replaced with oral hypoglycemic compounds when both blood glucose levels and corticosteroid dose have decreased. Patient education is essential, particularly for the management of hypoglycemia when corticosteroids are withdrawn or their dose tapered.