Aims/hypothesis. Impaired glucose tolerance (IGT) is an insulin-resistant state and a risk factor for Type 2 diabetes. The relative roles of insulin resistance and insulin deficiency in IGT have been disputed. Methods. In 40 IGT subjects and 63 sex-, age-, and weight-matched controls with normal glucose tolerance (NGT), we measured (i) indices of insulin sensitivity of fasting glucose production (by tracer glucose) and glucose disposal (M value on a 240 pmol·min -1 ·m -2 insulin clamp) and (ii) indices of beta-cell function (glucose sensitivity, rate sensitivity, and potentiation) derived from model analysis (Am J Physiol 283:E1159-E1166, 2002) of the insulin secretory response (by C-peptide deconvolution) to oral glucose. Results. In comparison with NGT, IGT were modestly insulin resistant (M=29±2 vs 35±2 µmol·min −1 ·kg FFM −1 , p=0.01); insulin sensitivity of glucose production also was reduced, in approximate proportion to M. Despite higher baseline insulin secretion rates, IGT was characterized by a 50% reduction in glucose sensitivity [53 (36) concept has evolved that in IGT, a mixture of insulin resistance and insulin deficiency is responsible for the abnormal rise in postglucose plasma glucose concentrations [12,13]. However, many previous studies of IGT have based conclusions on the measurement of plasma insulin concentrations rather than true insulin secretion rates. More importantly, to what extent insulin response to intravenous glucose reflects the insulin secretory response to oral glucose or mixed meals remains uncertain. In studies using graded glucose infusions and the C-peptide deconvolution technique to reconstruct insulin secretory rates, one study [14] documented a slower rise in insulin secretion as a function of rising plasma glucose concentrations in IGT subjects in comparison with subjects with normal gluImpaired glucose tolerance (IGT) is a condition of high risk for the development of Type 2 diabetes. Early physiological studies consistently showed that IGT is an insulin-resistant state [1,2,3,4,5] and documented the presence of impaired insulin response to intravenous glucose [6,7,8,9,10,11]. The general