Elevated basal insulin secretion and normal dynamic insulin sensitivity inborderline hypertension

Background and Aim: Borderline hypertension is often the initial stage of s tabilized hypertension. This study aimed to provide insight on insulin beha vior and its relationship with glucose metabolism by investigating insulin secretion and hepatic clearance in non-steady-state conditions in borderlin e hypertensive patients. Methods and Results: We studied 15 patients (6 F, 9M, 44+/-2 yr, 78+/-2 kg, systolic pressure 155+/-10 mmHg, diastolic 93+/-5) and 15 comparable healt hy controls. All underwent an intravenous glucose test, with minimal model analysis to measure insulin sensitivity S-1, glucose effectiveness S-G, ins ulin prehepatic release, hepatic extraction, and insulin appearance rate in the systemic circulation. Basal glucose (3.98+/-0.12 vs 3.94+/-0.11 mmol/L , hypertensive vs control subjects respectively), iv glucose tolerance fact or K-G (2.0+/-0.2 vs 2.2+/-0.1% min(-1)), SG (0.035+/-0.004 vs 0.032+/-0.00 7 min(-1)) and S-1 [3.5+/-0.5 vs 3.8+/-0.3 10(4) min(-1) (mu U/mL)] were si milar both basal insulin and C-peptide exhibited a marked increase (87+/-8 vs 46+/-6 pmol/L, p=0.0003; 637+/-62 vs 381+/-76 pmol/L, p<0.03) demonstrat ing insulin resistance in basal conditions. Insulin secretion per unit volu me was greater in patients, both at basal (43+/-5 vs 24+/-5 pmol/L/min, p=0 .01) and after stimulation (total hormone released = 18+/-2 vs 11+/-2 nmol/ L in 4h, p=0.022). Post-hepatic insulin delivery was also elevated (basal = 11+/-1 vs 6+/-1 pmol/L/min, p<0.002, total = 5+/-1 vs 3+/-0.3 nmol/L in 4h , p=0.02), while no difference was detected in hepatic extraction (66+/-4% vs 66+/-3). Conclusion: Borderline hypertensive patients display normal glucose toleran ce with basal insulin resistance and normal dynamic insulin sensitivity. Pe ripheral hyperinsulinemia derives from the combination of normal hepatic ex traction with an overproduction of hormone, mostly due to the basnl compone nt. Because borderline hypertension often degenerates into overt disease, o ur results point to a progression that leans to the well-known insulin resi stance proper to sustained hypertension.