Type 2 diabetes mellitus is a heterogeneous disorder characterized by chron
ic hyperglycaemia. The aetiological heterogeneity is suggested by genetic i
nheritance and its interplay with environmental factors. Impaired insulin s
ecretion 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 insuli
n 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.