Objective: To determine whether defects underlying impaired fasting glucose (IFG) are maintained and additive when combined with impaired glucose tolerance (IGT) (representing a progressive form of pre-diabetes), or are distinct in IFG/IGT (reflecting a parallel form of pre-diabetes). Methods: Volunteers with IFG (n=10), IFG/IGT (n=14), or normal glucose tolerance (NGT; n=15) were matched for demographics and anthropometry. Insulin secretion was assessed using the glucose step-up protocol and insulin action through the use of a 2-stage hyperinsulinemic-euglycemic clamp with infusion of [6,6-²H₂]-glucose. Results: Modeling of insulin secretory parameters revealed similar basal (_b), but diminished dynamic (_d), components in both IFG and IFG/IGT (p=0.05 vs. NGT for both). Basal glucose rate of appearance (Ra) was higher in IFG compared to NGT (p<0.01) and also, surprisingly, to IFG/IGT (p<0.04). Moreover, glucose Ra suppressed more during the low-dose insulin clamp in IFG (p<0.01 vs. NGT, p=0.08 vs. IFG/IGT). Insulin-stimulated glucose uptake (glucose rate of disappearance (Rd)) was similar in IFG, IFG/IGT and NGT throughout the clamp. Conclusions: Nuances of beta cell dysfunction observed in IFG were also noted in IFG/IGT. A trend for additional insulin secretory defects was observed in IFG/IGT, suggesting progression in beta cell failure in this group. In contrast, basal glucose Ra and its suppressability with insulin were higher in IFG, but not IFG/IGT, compared to NGT. Together, these data indicate that IFG/IGT may be a distinct pre-diabetic syndrome, rather than progression from IFG.