Results: A 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, where as 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.
Main Outcome Measures: Change in acute insulin secretory response assessed during hyperglycemicclamps while in sodium balance during a low-sodium vs high-sodium diet during aldosterone vs vehicle.
Conclusions: Low dietary sodium intake reduces insulin secretion in humans, independent of insulin sensitivity.
Context: Interruption of the renin-angiotensin-aldosterone system prevents incident diabetes in high-risk individuals, although the mechanism remains unclear.
Objective: To test the hypothesis that activation of the endogenous renin-angiotensin-aldosterone system or exogenous aldosterone impairs insulin secretion in humans.
Design: We conducted a randomized, blinded crossover study of aldosterone vs vehicle and compared the effects of a low-sodium versus a high-sodium diet.
Setting: Academic clinical research center.
Participants: Healthy, nondiabetic, normotensive volunteers.
Interventions: Infusion 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.
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism
- Clinical Biochemistry
- Biochemistry, medical