Horm Metab Res 1999; 31(9): 533-536
DOI: 10.1055/s-2007-978789
Original Clinical

© Georg Thieme Verlag Stuttgart · New York

Leptin Levels are Suppressed in Primary Aldosteronism

D. J. Torpy1 , S. R. Bornstein1 , W. Taylor2 , R. Tauchnitz3 , R. D. Gordon2
  • 1Developmental Endocrinology Branch, National Institutes of Health, Bethesda, MD, USA
  • 2Hypertension Unit, University of Queensland Department of Medicine, Greenslopes Hospital, Brisbane, Qld, Australia
  • 3Department of Medicine, University of Leipzig, Leipzig, Germany
Further Information

Publication History

1999

1999

Publication Date:
20 April 2007 (online)

Primary aldosteronism is associated with hypertension secondary to salt and water retention, hypokalemia and impaired insulin secretion with glucose intolerance in some patients. The secretion of leptin, a hormone produced by adipocytes, may be altered by reduced insulin secretion in primary aldosteronism. We measured plasma leptin approximately 3 months before and 3 months after curing of primary aldosteronism in 18 patients (12 male, 6 female, body mass index 29.1 ± 4.4, mean ± SD). Patients were treated by unilateral laparoscopic adrenalectomy to remove an aldosterone-producing adenoma. There was a 46% postoperative increase in plasma leptin concentrations from 6.65 ± 0.81 to 9.68 ± 1.50 ng/ml (P = 0.004), despite a non-significant fall in body mass index. Plasma leptin was noted to increase after adrenalectomy in 16 of the 18 patients. The patients also had improved blood pressure and a significant increase in plasma potassium post-operatively. It is proposed that increased insulin secretory capacity associated with correction of negative potassium balance may account for the increase in plasma leptin after curing primary aldosteronism. Further studies are indicated to identify the mechanism of plasma leptin suppression in primary aldosteronism.

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