To clarify the event that is involved in the pathogenesis of impaired glucose tolerance (IGT), we studied 15 individuals with IGT and 15 subjects with normal tolerance using the minimal model approach. Our IGT subjects were characterized by normal insulin secretory responses to oral glucose and mild impairments in insulin sensitivity (SI) and glucose effectiveness (SG) at basal and zero insulin. Next, we classified our IGT subjects into two subpopulations: one with normal insulin sensitivity (SI: 0.92 ± 0.11 × 10(−4) min−1 · pmol/l−1 and the other with insulin resistance (SI: 0.31 ± 0.06 × 10−4 min−1 · pmol/l−1, P < 0.05). The populations did not differ with respect to body mass index and fasting plasma glucose level. Basal plasma insulin level was higher in the insulin-resistant group (84.8 ± 23.3 pmol/l) than in the insulin-sensitive group (48.7 ± 6.8 pmol/l), but the difference was not statistically significant. The absolute insulin secretory responses to oral glucose were significantly higher in the resistant group (83,205 ± 17,787 pmol/l × min) than in the sensitive group (24,727 ± 3,591 pmol/l × min, P < 0.01), whose absolute responses were similar to those of normal control subjects (24,576 ± 2,767 pmol/l × min). No significant difference was observed in SG between the resistant (0.016 ± 0.002 min−1) and sensitive (0.013 ± 0.002 min−1, P > 0.05) type of IGT, but SG was significantly type of IGT, but SG was significantly decreased in both groups compared with normal control subjects (0.023 ± 0.002 min−1, P < 0.05–0.01). particular population is composed of at least two sub-populations: one with insulin resistance and higher insulin response to oral glucose and the other with normal insulin sensitivity and normal insulin response to oral glucose. In both, SG was significantly impaired compared with normal control subjects.

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