Type 2 diabetes mellitus is a heterogeneous disorder with genetic and acquired components. It is primarily due to impaired insulin secretion in that individuals with genetically impaired beta cell function cannot increase their insulin release sufficiently to compensate for insulin resistance. The resultant hyperglycemia is largely the consequence of excessive release of endogenous 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 (thiazolidinediones) insulin sensitivity are effective treatments for the condition.