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This Article Full Text Full Text (PDF) All Versions of this Article: 295/2/E428    most recent 90354.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Perreault, L. Articles by Eckel, R. H. PubMed PubMed Citation Articles by Perreault, L. Articles by Eckel, R. H.

Impaired fasting glucose with or without impaired glucose tolerance: progressive or parallel states of prediabetes?

¹Division of Endocrinology, Metabolism, and Diabetes, University of Colorado Health Sciences Center, Aurora, Colorado; and ²Department of Information Engineering, University of Padua, Padua, Italy

Submitted 10 April 2008 ; accepted in final form 29 May 2008

Our objective was 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 prediabetes) or are distinct in IFG/IGT (reflecting a parallel form of prediabetes). 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 two-stage hyperinsulinemic euglycemic clamp with infusion of [6,6-²H₂]glucose. 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 (R_a) was higher in IFG compared with NGT (P < 0.01) and also, surprisingly, with IFG/IGT (P < 0.04). Moreover, glucose R_a 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 (R_d)] was similar in IFG, IFG/IGT, and NGT throughout the clamp. We conclude that nuances of β-cell dysfunction observed in IFG were also noted in IFG/IGT. A trend for additional insulin secretory defects was observed in IFG/IGT, possibly suggesting progression in β-cell failure in this group. In contrast, basal glucose R_a and its suppressability with insulin were higher in IFG, but not IFG/IGT, compared with NGT. Together, these data indicate that IFG/IGT may be a distinct prediabetic syndrome rather than progression from IFG.

insulin resistance; isotopes; clamp