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Body Mass Index Predicts Aldosterone Production in Normotensive Adults on a High-Salt Diet

Divisions of Endocrinology, Diabetes, and Hypertension (R.B.-L., G.K.A., E.W.S., G.H.W., R.G.) and Cardiology (T.P.), Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts 02115; and Division of Cardiology and Cardiovascular Genetics (P.N.H.), University of Utah, Salt Lake City, Utah 84112

Address all correspondence and requests for reprints to: Rajesh Garg, M.D., Brigham and Women’s Hospital, Division of Endocrinology, Diabetes, and Hypertension, 221 Longwood Avenue, Boston, Massachusetts 02115. E-mail: rgarg{at}partners.org.

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.

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