SFEBES2026 Oral Poster Presentations Adrenal and Cardiovascular (4 abstracts)
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 Vincents 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 Columcilles 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 chromatographytandem 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 (45.154.6); median age 50.5 years (43.356.6)]. Median weight loss after surgery was 17.6% (13.721.2) after 18 weeks (1620). 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 (115328), P = 0.002] and deoxycorticosterone concentrations [100pmol/l (0.00100) to 85pmol/l (53127), P = 0.05], with a non-significant reduction in urinary tetrahydroaldosterone concentrations. Serum corticosterone increased following weight loss [5.5nmol/l (3.29.95) to 9.3nmol/l (4.516.8), P = 0.001]. Postoperative increases were observed in urinary tetrahydrocorticosterone [136 (86208) to 167 (120279) mg/24h, P = 0.0123] and tetrahydrodeoxycorticosterone [148 (55269) to 222 (83380) 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.