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Submitted on May 15, 2007
Accepted on August 21, 2007
Division of Endocrinology, Diabetes, and Hypertension and Brigham and Women's Hospital and Harvard Medical School, Boston, MA, Division of Cardiology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, Division of Cardiology, Cardiovascular Genetics, University of Utah, Salt Lake City, UT
* To whom correspondence should be addressed. E-mail: rgarg{at}partners.org.
Context: The mechanisms underlying obesity-mediated cardiovascular disease are not fully understood. Aldosterone and insulin resistance 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 high sodium diet.
Participants/Interventions: Healthy normotensive adults were categorized as "lean" body mass index (BMI) < 25 kg/m2 (n = 63) or "overweight" BMI 
25 kg/m2 (n = 57). After 7 days 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 to the lean group had higher twenty-four hour urinary aldosterone (9.0 ± 0.8 vs. 6.6 ± 0.5 µg/24 hrs; 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-hr urinary cortisol or sodium, or in 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 to 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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