Abstract

OBJECTIVE: Primary aldosteronism (PA) is the most common secondary cause of hypertension and recently has been implicated as a cause of impaired glucose tolerance. We investigated the glucose insulin sensitivity and insulin secretion in patients with idiopathic primary aldosteronism. DESIGN: Thirty PA patients and 60 essential hypertensive (EH) patients as controls were included, matched (1: 2) by their body mass index (BMI) (29.9 ± 4.3 versus 29.8 ± 5.8 m/kg), age (53.7 ± 9.4 versus 59.9 ± 8.6 years old) and gender (male/female: 8/22 versus 17/43). In all patients, we measured insulin, total cholesterol, triglycerides, C-peptide and fasting glucose levels. Homeostasis model assessment for insulin resistance (HOMA-IR) and HOMA of pancreatic β-cell function (HOMA-βF) indexes were calculated. We also evaluated the response to spironolactone in 19 PA patients. RESULTS: PA patients had higher levels of glucose (5.2 ± 0.7 versus 4.9 ± 0.7 mmol/l; P = 0.017). Insulin levels (10.7 ± 6.5 versus 11.5 ± 5.8 uUI/ml, P = 0.525) and HOMA-IR (2.51 ± 1.59 versus 2.45 ± 1.29 uUI/ml x mmol/l, P = 0.854) were similar in both groups. HOMA-βF index (138.9 ± 89.8 versus 179.8 ± 100.2%, P = 0.049) and C-peptide (0.83 ± 0.63 versus 1.56 ± 0.84 ng/dl, P = 0.0001) were lower in PA patients. Potassium was normal in both groups. Negative correlations between serum aldosterone/plasma renin activity (SA/PRA) ratio and HOMA-βF, and between C-peptide and SA levels were found in all patients. After the spironolactone treatment, we found an increase of C-peptide and insulin levels without changes in HOMA-IR or HOMA-βF. CONCLUSION: Our results showed differences in glucose metabolism between PA patients and those with hypertension suggesting that these findings could probably be determined by a lower β-cell function influenced by aldosterone. These findings highlight the importance of aldosterone in glucose metabolism. © 2007 Lippincott Williams & Wilkins, Inc.