|| Checking for direct PDF access through Ovid
To determine whether kinetic abnormalities in the onset of insulin action contribute to the insulin resistance in obesity-associated hypertension.We monitored the rate of increase in glucose infusion during 6 h of hyperinsulinemic (40 mU/m2 per min) euglycemic clamps in hypertensive and normotensive obese subjects. The two groups of hypertensive (n = 9) and normotensive (n = 9) subjects were matched for age (48 ± 2 versus 45 ± 5 years), sex (five males and four females versus four males and five females) and body mass index (42 ± 3 versus 40 ± 2 kg/m2).In all subjects, the glucose infusion rate required to maintain euglycemia increased progressively during the clamp studies to achieve maximal, steady-state values within the fifth hour. During the first 2 h of the clamp, mean glucose infusion rate, the traditional approach to assessing insulin sensitivity, was lower in the hypertensive than in the normotensive obese patients (2.04 ± 0.13 versus 3.29 ± 0.41 mg/kg per min, respectively; P < 0.05). In contrast, the maximal steady-state glucose infusion rate, calculated as the mean value during the sixth hour of clamping, was similar in the hypertensive and in the normotensive obese patients (4.48 ± 0.43 versus 4.81 ± 0.45 mg/kg per min, respectively; NS). The time required to reach the half-maximal glucose infusion rate was greater in the hypertensive than normotensive obese patients (91 ± 12 versus 38 ± 5 min, respectively; P < 0.05).In obesity, hypertension was associated with a slower rate of activation of the insulin effect on glucose metabolism, whereas the maximal steady-state insulin effects were not altered by elevated blood pressure. Thus, the link between obesity and hypertension may be associated with the kinetics of onset of insulin action.