The therapy of type 2 diabetes mellitus is symptomatic—the immediate treatment goal remains the day-to-day management of hyperglycaemia and the restoration of glycaemic control. This is preferably achieved with minimal risk of hypoglycaemia and without further weight gain in subjects who are often obese. Principal treatment goals for successful long-term glucose management include reduced comorbidities and mortality (particularly through reduced mirco-, and, to some extent, macrovascular risk) along with an alleviation of any presenting diabetic symptomology, including susceptibility to infection, fatigue, thirst and polyuria. To this end, a chemically diverse range of oral antidiabetic agents can be used, singly or in combination, against a range of molecular targets in an attempt to: limit or delay glucose absorption from the gut (with alpha-glucosidase inhibitors, anti-absorptive ‘starch blockers’); enhance pancreatic insulin release (using sulphonylurea and glinide class insulin secretagogues, as well as the gliptin class incretin enhancers); depress hepatic glucose production (principally with the biguanide class, but also with the use of glitazones and gliptins); enhance peripheral insulin sensitivity/insulin receptor signalling (with the glitazone and biguanide classes); and most recently, prevent glucose reabsorption from the renal filtrate (with the novel gliflozin class of glucose ‘wasters’).