Body mass index predicts aldosterone production in normotensive adults on a high-salt diet

R Bentley-Lewis, GK Adler, T Perlstein… - The Journal of …, 2007 - academic.oup.com
R Bentley-Lewis, GK Adler, T Perlstein, EW Seely, PN Hopkins, GH Williams, R Garg
The Journal of Clinical Endocrinology & Metabolism, 2007academic.oup.com
Context: The mechanisms underlying obesity-mediated cardiovascular disease are not fully
understood. Aldosterone and insulin resistance both are associated with obesity and
cardiovascular disease. Objectives: The objectives of this study were to test the hypotheses
that aldosterone production is elevated and associated with insulin resistance in overweight
adults on a high-sodium diet. Participants/Interventions: Healthy normotensive adults were
categorized as lean body mass index (BMI) less than 25 kg/m2 (n= 63) or overweight BMI 25 …
Abstract
Context: The mechanisms underlying obesity-mediated cardiovascular disease are not fully understood. Aldosterone and insulin resistance both are associated with obesity and cardiovascular disease.
Objectives: The objectives of this study were to test the hypotheses that aldosterone production is elevated and associated with insulin resistance in overweight adults on a high-sodium diet.
Participants/Interventions: Healthy normotensive adults were categorized as lean body mass index (BMI) less than 25 kg/m2 (n = 63) or overweight BMI 25 kg/m2 or greater (n = 57). After 7 d of a high-sodium diet, participants fasted overnight and remained supine throughout hemodynamic and laboratory assessments and angiotensin II (AngII) stimulation.
Results: The overweight group, compared with the lean group, had higher 24-h urinary aldosterone (9.0 ± 0.8 vs. 6.6 ± 0.5 μg per 24 h; P = 0.003) and higher AngII-stimulated serum aldosterone (11.4 ± 1.0 vs. 9.0 ± 0.6 ng/dl; P = 0.04). There were no differences in 24-h urinary cortisol or sodium or supine measurements of plasma renin activity, serum aldosterone, or serum potassium. The homeostasis model assessment of insulin resistance was predicted by urinary aldosterone excretion (r = 0.32, P = 0.03) and serum aldosterone response to AngII stimulation (r = 0.28, P = 0.02) independent of age and BMI.
Conclusion: Urinary aldosterone excretion and AngII-stimulated aldosterone are increased in overweight, compared with lean, normotensive adults. The correlation of these measures of aldosterone production with insulin resistance suggests a potential role for aldosterone in the pathophysiology of obesity-mediated insulin resistance.
Oxford University Press