Type 2 diabetes mellitus is a heterogeneous disorder with genetic and acqui
red components. It is primarily due to impaired insulin secretion in that i
ndividuals with genetically impaired beta cell function cannot increase the
ir insulin release sufficiently to compensate for insulin resistance. The r
esultant hyperglycemia is largely the consequence of excessive release of e
ndogenous glucose due to increased gluconeogenesis. Nevertheless, clinical
experience has demonstrated that therapies directed at improving beta cell
function (sulfonylureas) and at improving hepatic (metformin) and muscle (t
hiazolidinediones) insulin sensitivity are effective treatments for the con
dition.