Interaction between glucose metabolism and endogenous insulin release in hypertension

The minimal model approach was applied to examine the dynamic interaction between glucose metabolism and endogenous insulin release during an intravenous glucose tolerance test (IVGTT) in a group of hypertensive patients (H group) compared with a group of normotensive subjects (N group). A modified version of the classical minimal model of C-peptide kinetics and secretion was used to evaluate the total amount of insulin secretion per unit of distribution volume (TIS) together with 3 indexes of beta-cell function (the basal, Phi(b), first, Phi1, and second phase, Phi2, beta-cell sensitivity to glucose). These indexes were associated with estimates of glucose effectiveness (S(G)) and insulin sensitivity (S(I)) provided by the classical minimal model of glucose kinetics. No significant differences were found in Phi(b), Phi1, and Phi2 estimates between the H group and the N group. In the H group, the average TIS was 54% higher (P <.05) than in the N group, while S(G) and S(I) estimates showed a 44% decrease (P <.05) and a 51% decrease (P <.05), respectively. These results suggest that hyperglycemia observed in our H group during IVGTT is a compensatory response to insulin resistance (low S(I)) and to the reduced ability of glucose to promote its own metabolism (low S(G)). This hyperglycemic state causes a larger than normal stimulation of beta cell, which explains insulin hypersecretion (higher TIS) even in the presence of normal beta-cell sensitivity values of Phi(b), Phi1, and Phi2.