Abstract

Primary aldosteronism is associated with an increased risk of diabetes, but the mechanism is uncertain. We enrolled 9 patients with primary aldosteronism and assessed insulin secretion and insulin sensitivity beforte and after 3-12 months after either adrenalectomy (n-6) or medical treatment (n=3). Plasma 8AM Aldosterone ( p =0.02) and 11-deoxycorticosterone ( p =0.02) decreased after treatment, whereas cortisol was unchanged ( p =0.57). Systolic blood pressure (131.1±3.6 vs 124.3±7.7; p =0.43), serum potassium (3.7±0.1 vs 4.1±0.1 mEq/L; p =0.063), and creatinine (1.1±0.1 vs 1.2±0.1 mg/dL; p =0.35) were similar after treatment. During hyperglycemic clamps, we infused glucose to increase plasma glucose to a target of 200mg/dL ( a ). The insulin response ( b , 218.6±39.8 vs 403.1±42.0 pM insulin mean at 90-120 min, p =0.004) and L-arginine stimulated insulin response ( c) increased compared to Pre-Treatment assessment. C-peptide results were similar to insulin alterations. Comparison to control subjects matched for age, race, sex, and BMI ( Figure , gray line and area indicating mean±95%CI) indicated that insulin secretion after treatment was comparable to healthy individuals. During hyperinsulinemic-euglycemic clamps, insulin clearance (steady state insulin divided by insulin infusion rate) increased after treatment (855±68 vs 615±57 mL/min, p =0.031). Insulin sensitivity decreased after treatment (30.7±2.1 vs 18.5±1.6 M/I; p =0.016), but disposition index was unchanged (acute insulin response x M/I; p =0.81).

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