The diagnostic categories of impaired glucose tolerance (IGT) and impaired 
fasting glucose (IFG) were stablished in an effort to identify populations at 
risk for developing type 2 diabetes mellitus (T2DM). Both IGT and IFG are 
associated with increased risk of developing T2DM, but recent analyses found 
that the thresholds of risk vary among different populations and an even lower 
diagnostic threshold of IFG may be appropriate. IGT has been linked with an 
increased risk of cardiovascular events and some analyses have demonstrated an 
increased mortality risk compared with patients with normal glucose tolerance. 
In contrast, a continuum of increased risk of microvascular manifestations of 
T2DM has been demonstrated with IFG but an association of IFG with 
cardiovascular events has not been well established. Although both IGT and IFG 
are associated with resistance to insulin and increased insulin secretion, they 
do not identify the identical patient populations and are not equivalent in 
predicting development of T2DM or cardiovascular events. IFG and IGT have been 
associated with other features of insulin resistance, including dyslipidaemia, 
hypertension, abdominal obesity, microalbuminuria, endothelial dysfunction, and 
markers of inflammation and hypercoagulability, traits collectively referred to 
as the metabolic syndrome. Analyses of combinations of these components have 
also been associated with progression to T2DM, cardiovascular disease and 
increased mortality. The foundation of treatment for IGT, IFG, and the metabolic 
syndrome is lifestyle modification, including both dietary change and routine 
exercise. To date, several clinical trials have found that lifestyle 
modification is the most efficacious strategy to prevent progression to T2DM. 
Alternative treatments include pharmacotherapy with metformin or acarbose, both 
of which have been demonstrated to decrease the development of T2DM. Ongoing 
clinical trials are evaluating newer pharmacotherapies, including angiotensin 
converting enzyme inhibitors, angiotensin receptor antagonists, metglitinides 
and thiazolidinediones, to prevent both T2DM and cardiovascular events. In 
combination with lifestyle modification, these therapies offer hope for 
effective prevention of T2DM and its consequences in high-risk patients.