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J Clin Endocrinol Metab. 2013 Jun;98(6):2513-20. doi: 10.1210/jc.2012-3934. Epub 2013 Mar 28.

Aldosterone excess impairs first phase insulin secretion in primary aldosteronism.

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Medizinische Klinik und Poliklinik IV, Klinikum der Universität München, Ziemssenstrasse 1, 80336 München, Germany.



Primary aldosteronism (PA) represents the most frequent cause of secondary arterial hypertension. Conflicting data have been published regarding the effect of aldosterone excess on glucose metabolism.


Our aim was to analyze insulin sensitivity and β-cell function in a cohort of PA patients. Prospective follow-up investigations were performed in a subgroup of patients before and after adrenalectomy to assess the metabolic outcome.


Oral glucose tolerance test, combined intravenous glucose tolerance test, hyperinsulinemic-euglycemic glucose clamp test, and arginine test were carried out after a 12-hour fasting period.


Twenty-two consecutive patients with both unilateral aldosterone-producing adenoma and bilateral idiopathic adrenal hyperplasia were recruited through the Munich center of the German Conn's Registry. The control group of patients with essential hypertension (n = 11) of corresponding age and body mass index was recruited from our hypertension unit. A normotensive cohort (n = 11) served as a further control group.


At baseline, first-phase insulin reaction in intravenous glucose tolerance test was significantly reduced in patients with PA as compared to normal controls (36.0 [24.0; 58.7] vs 90.1 [52.6; 143.8] μU/mL, P = .031) and lower in comparison to essential hypertension without reaching statistical significance (53.2 [30.8; 73.3] μU/mL, P = .123). The study was repeated 6 months after unilateral adrenalectomy in 9 consecutive patients with aldosterone-producing adenoma. At this time point, blood pressure had been normalized in most of the patients while body mass index remained unchanged (26.9 [25.5; 37.6] vs 27.5 [25.1; 35.6] kg/m(2), P = .401). First-phase insulin reaction in response to glucose significantly increased at follow-up (from 36.0 [25.5; 58.7] to 48.5 [40.4; 95.2] μU/mL, P = .038, n = 9). In contrast, insulin sensitivity and response to iv arginine did not differ before and after adrenalectomy.


Aldosterone excess has a direct negative effect on β-cell function in patients with PA. After adrenalectomy, glucose-induced first-phase insulin secretion improves significantly in the patients.

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