ABSTRACT
Glucose clamp experiments have shown that patients with reactive postprandial hypoglycaemia (PRH) frequently have an increased glucose disposal, but the relative involvement of insulin sensitivity (SI) and glucose effectiveness (Sg) in this process remains unknown. The minimal model approach was used to compare 13 patients in whom moderate reactive hypoglycaemia ( < 3.3 mmol) had been previously diagnosed and 13 matched controls. The intravenous glucose tolerance test (IVGTT, 0.5 g/kg glucose IV) with 0.02 U/kg insulin given at the 19th min and frequent sampling over 180 min shows that PRH patients exhibit a higher glucose tolerance coefficient Kg (2.99 +/- 0.26 vs 2.19 +/- 0.12; P < 0.02), higher SI [22.9 +/- 6.4 vs 7.18 +/- 0.14 min-1/(microU/ml). 10(-4); P < 0.01] and higher Sg (3.84 +/- 0.35 vs 2.92 +/- 0.79 min-1. 10(-2); P < 0.05). The increase in Sg is explained by an increase in its component basal insulin effectiveness (BIE: 1.2 +/- 0.27 min-1.10(-2) in PRH subjects vs 0.58 +/- 0.07; P < 0.05) rather than an increase in Sg at zero insulin. The increase in BIE results from the high values of SI. In 4 PRH subjects SI and Sg were within the normal range, and the increase in Kg evidenced in the 9 others was explained by an increase in SI alone in 3 cases, in Sg alone in 1 case, and both SI and Sg in 5 cases. Thus, in sedentary subjects, the previously reported rise in tissue glucose assimilation is mainly explained by an increased insulin-mediated glucose disposal rather than non-insulin-mediated glucose disposal.
