• James M Luther, Loretta M Byrne, Chang Yu, Thomas J Wang, and Nancy J Brown.
• Divisions of Clinical Pharmacology, Department of Medicine (J.M.L., L.M.B., N.J.B.), Nephrology and Hypertension (J.M.L.), and Cardiovascular Medicine (T.J.W.), and Departments of Biostatistics (C.Y.) and Pharmacology (J.M.L.), Vanderbilt University Medical Center, Nashville, Tennessee 37232-6602.
• J. Clin. Endocrinol. Metab. 2014 Oct 1; 99 (10): E1895-902.

ContextInterruption of the renin-angiotensin-aldosterone system prevents incident diabetes in high-risk individuals, although the mechanism remains unclear.ObjectiveTo test the hypothesis that activation of the endogenous renin-angiotensin-aldosterone system or exogenous aldosterone impairs insulin secretion in humans.DesignWe conducted a randomized, blinded crossover study of aldosterone vs vehicle and compared the effects of a low-sodium versus a high-sodium diet.SettingAcademic clinical research center.ParticipantsHealthy, nondiabetic, normotensive volunteers.InterventionsInfusion of exogenous aldosterone (0.7 μg/kg/h for 12.5 h) or vehicle during low or high sodium intake. Low sodium (20 mmol/d; n = 12) vs high sodium (160 mmol/d; n = 17) intake for 5-7 days.Main Outcome MeasuresChange in acute insulin secretory response assessed during hyperglycemic clamps while in sodium balance during a low-sodium vs high-sodium diet during aldosterone vs vehicle.ResultsA low-sodium diet increased endogenous aldosterone and plasma renin activity, and acute glucose-stimulated insulin (-16.0 ± 5.6%; P = .007) and C-peptide responses (-21.8 ± 8.4%; P = .014) were decreased, whereas the insulin sensitivity index was unchanged (-1.0 ± 10.7%; P = .98). Aldosterone infusion did not affect the acute insulin response (+1.8 ± 4.8%; P = .72) or insulin sensitivity index (+2.0 ± 8.8%; P = .78). Systolic blood pressure and serum potassium were similar during low and high sodium intake and during aldosterone infusion.ConclusionsLow dietary sodium intake reduces insulin secretion in humans, independent of insulin sensitivity.

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