Elevated basal insulin secretion and normal dynamic insulin sensitivity in borderline hypertension

Borderline hypertension is often the initial stage of stabilized hypertension. This study aimed to provide insight on insulin behavior and its relationship with glucose metabolism by investigating insulin secretion and hepatic clearance in non-steady-state conditions in borderline hypertensive patients.

We studied 15 patients (6 F, 9M, 44 +/- 2 yr, 78 +/- 2 kg, systolic pressure 155 +/- 10 mmHg, diastolic 93 +/- 5) and 15 comparable healthy controls. All underwent an intravenous glucose test, with minimal model analysis to measure insulin sensitivity S1, glucose effectiveness SG, insulin pre-hepatic 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), i.v. glucose tolerance factor KG (2.0 +/- 0.2 vs 2.2 +/- 0.1% min-1), SG (0.035 +/- 0.004 vs 0.032 +/- 0.007 min-1) and S1 [3.5 +/- 0.5 vs 3.8 +/- 0.3 10(4) min-1 (microU/mL)] were similar, 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) demonstrating insulin resistance in basal conditions. Insulin secretion per unit volume 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 4 h, 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 4 h, p = 0.02), while no difference was detected in hepatic extraction (66 +/- 4% vs 66 +/- 3).

Borderline hypertensive patients display normal glucose tolerance with basal insulin resistance and normal dynamic insulin sensitivity. Peripheral hyperinsulinemia derives from the combination of normal hepatic extraction with an overproduction of hormone, mostly due to the basal component. Because borderline hypertension often degenerates into overt disease, our results point to a progression that leads to the well-known insulin resistance proper to sustained hypertension.