Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2026) 117 OP3.4 | DOI: 10.1530/endoabs.117.OP3.4

SFEBES2026 Oral Poster Presentations Adrenal and Cardiovascular (4 abstracts)

Weight loss induced by bariatric surgery impacts significantly on serum and urinary mineralocorticoid metabolism in men and women

Clare Miller 1,2 , Talal Saad Almukhlifi 3,4 , Tara McDonnell 1,2 , Leanne Cussen 1,2 , Maria Tomkins 1,2 , Angela E. Taylor 5 , Marie McIlroy 1 , Jean O’Connell 3,6 , Helen Heneghan 3,6 , Donal O’Shea 3,6 , Wiebke Arlt 7 , Mark Sherlock 1,2 & Michael W. O’Reilly 1,2


1Androgens in Health and Disease Research Group, Department of Medicine, Royal College of Surgeons, Dublin, Ireland; 2Department of Endocrinology, Beaumont Hospital, Dublin, Ireland; 3Department of Bariatric Surgery, St Vincent’s University Hospital, Dublin, Ireland; 4Department of Surgery, Prince Sttam Bin Abdulaziz University, Al-Kharj City, Saudi Arabia; 5Steroid Metabolomics Analysis Core, Department of Metabolism and Systems Science, University of Birmingham, Birmingham, United Kingdom; 6Centre for Obesity Management, St Columcille’s Hospital, Dublin, Ireland; 7Medical Research Council Laboratory of Medical Sciences, London, United Kingdom


Obesity is a risk factor for hypertension and perturbations in mineralocorticoid metabolism have been implicated. Weight loss reduces aldosterone concentrations without parallel changes in renin activity, implicating renin-independent mechanisms. Adipocytes express aldosterone synthase (CYP11B2) and secrete aldosterone, providing a potential mechanism linking adiposity to mineralocorticoid metabolism. Robust data exploring this association using highly sensitive liquid chromatography–tandem mass spectrometry (LC-MS/MS) methods are lacking. Baseline anthropometric and metabolic data were collected in a cohort of patients undergoing bariatric surgery for obesity. Serum and urine samples were collected for multisteroid profiling by LC-MS/MS pre-operatively. Clinical and biochemical assessments were repeated after a defined postoperative interval. Data are reported as median and interquartile range. Sixty-two patients were included [n = 41 female; median BMI 49.3kg/m2 (45.1–54.6); median age 50.5 years (43.3–56.6)]. Median weight loss after surgery was 17.6% (13.7–21.2) after 18 weeks (16–20). Blood pressure improved [systolic 140±14 mmHg to 132±13mmHg; diastolic 83±11 mmHg to 77 ± 12 mmHg, P < 0.05 for each]; antihypertensive medication use fell in study participants from 53.2% to 32.3%. Weight loss significantly reduced serum aldosterone [300pmol/l (200-500) to 175pmol/l (115–328), P = 0.002] and deoxycorticosterone concentrations [100pmol/l (0.00–100) to 85pmol/l (53–127), P = 0.05], with a non-significant reduction in urinary tetrahydroaldosterone concentrations. Serum corticosterone increased following weight loss [5.5nmol/l (3.2–9.95) to 9.3nmol/l (4.5–16.8), P = 0.001]. Postoperative increases were observed in urinary tetrahydrocorticosterone [136 (86–208) to 167 (120–279) mg/24h, P = 0.0123] and tetrahydrodeoxycorticosterone [148 (55–269) to 222 (83–380) mg/24h, P = 0.0004]. The concurrent fall in aldosterone and rise in corticosterone may indicate altered CYP11B2 activity, with increased urinary tetrahydro-metabolites suggesting enhanced hepatic clearance from higher substrate availability. These data suggest mineralocorticoid excess contributes to obesity-related hypertension and is potentially ameliorated by weight loss.

Volume 117

Society for Endocrinology BES 2026

Harrogate, United Kingdom
02 Mar 2026 - 04 Mar 2026

Society for Endocrinology 

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