1 From the Division of Pediatric Cardiology, University of Minnesota, Minneapolis, Minnesota
2 From the Division of Pediatric Cardiology, Departments of Pediatrics and Kinesiology, University of Michigan, Ann Arbor, Michigan
To determine if physiologic changes of insulin are capable of inducing sodium retention in insulin-resistant patients, we evaluated the ability of an oral glucose tolerance test to alter urine sodium excretion in 32 obese subjects (13.3 ± 1 years, weight 82 ± 5 kg, mean arterial pressure 89.3 ± 1.5 mm Hg) and 13 nonobese subjects (13.8 ± 2 years, weight 46 ± 4 kg, mean arterial pressure 74.5 ± 2.6 mm Hg).
After an overnight fast, subjects were placed in water diuresis and fasting insulin and glucose levels were drawn. Three 30-minute urine collections were obtained for baseline urine sodium excretion. The oral glucose tolerance test was administered with glucose and insulin levels drawn at 15, 30, 45, 60, 90, and 120 minutes. During the oral glucose tolerance test, four 30-minute urine collections were obtained for urine sodium excretion.
Serum glucose levels at baseline and throughout the glucose tolerance test did not differ between obese and nonobese subjects. Baseline insulin levels were elevated significantly in the obese (20 ± 3 µU/mL) compared with the nonobese (5 ± 0.7 µU/mL) subjects. Furthermore, insulin levels remained significantly elevated in the obese subjects compared with the nonobese subjects throughout the glucose tolerance test (118 ± 19 vs 49 ± 6 µU/mL, obese vs nonobese subjects at 1-hour post-glucose tolerance test). Prior to the oral glucose tolerance test, urine sodium excretion was not different between obese (249 ± 13 µEq/min) and nonobese (225 ± 28 µEq/min) subjects; however, during the oral glucose tolerance test there was a significant decrease in urine sodium excretion in the obese (158 ± 15 µEq/min) subjects, but no significant change in urine sodium excretion in the nonobese (221 ± 31 µEq/min) subjects.
The data support the hypothesis that, in the obese, changes in insulin associated with eating can result in sodium retention. This insulin-mediated sodium retention may participate in the development of hypertension in obese subjects.
Key Words: Insulin resistance urine sodium excretion salt sensitivity hypertension obesity
Submitted on February 4, 1992
Accepted on April 6, 1992