Insulin action and secretion in hypertension in the absence of metabolic syndrome: model-based assessment from oral glucose tolerance test.

Relationship between insulin action and secretion was analyzed in 10 hypertensive patients (H group; 5 male, 5 female; 56.9 +/- 2.5 years) compared with 10 normotensive subjects (N group; 5 male, 5 female; 51.7 +/- 3.7 years; P > .05) matched for age, sex, and body mass index. All participants (normoglycemic, nonobese, and not affected by metabolic syndrome) underwent a 5-hour, 22-sample, oral (75 g) glucose tolerance test. Insulin sensitivity was quantified by quantitative insulin sensitivity check index and an insulin sensitivity index computed by minimal-model-based "integral equation." beta-Cell responsivity indexes (dynamic, Phi(d); static, Phi(s); and global, Phi(oral)) were estimated by C-peptide oral minimal model. Compared with the N group, our H group featured no significant difference (P > .05) in fasting glycemia, significant (P < .02) increase in plasma insulin (93%) and C-peptide (53%) concentrations, and significant (P < .01) reduction in both quantitative insulin sensitivity check index (10%) and insulin sensitivity index (68%). No significant variations of mean Phi(d), Phi(s), and Phi(oral) were observed across the 2 groups in response to glucose challenge. Thus, insulin sensitivity deterioration in hypertension was not mirrored by a reciprocal change in beta-cell responsivity. Nevertheless, our H group featured a 143% (P < .005) increase in the area under the curve of circulating insulin and a 34% (P < .01) reduction in the ratio between the area under C-peptide curve and the area under the curve of circulating insulin. These results support the hypothesis that decreased insulin clearance in hypertensive patients, not affected by metabolic syndrome, is a further regulatory mechanism, in addition to increased insulin secretion, to compensate for insulin resistance.