Type 2 diabetes mellitus is a heterogeneous disorder characterized by chronic hyperglycaemia. The aetiological heterogeneity is suggested by genetic inheritance and its interplay with environmental factors. Impaired insulin secretion and decreased insulin sensitivity are the main pathophysiological features, responsible for development of hyperglycaemia in type 2 diabetes. However, the genetic basis of these defects has been demonstrated only in small subgroups of patients. Whether impaired secretion or action of insulin is the primary defect in the majority of patients is not known, although it is generally agreed that defective insulin release is a requirement for the disease to develop.