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.
Beta cell dysfunction - insulin resistance
