ESPE2024 Poster Category 1 Adrenals and HPA Axis 1 (9 abstracts)
Leptin and adiponectin are associated with the glucocorticoid dose and androgen concentrations in children and young persons with congenital adrenal hyperplasia: data from the CAH-UK cohort.
Irina A Bacila 1,2 , Neil R Lawrence 1 , Sabah Alvi 3 , Timothy D Cheetham 4,5 , Elizabeth Crowne 6 , Urmi Das 7 , Mehul T Dattani 8 , Justin H Davies 9 , Evelien Gevers 10,11 , Brian Keevil 12 , Ruth E Krone 13 , Allan Lawrie 14 , Leena Patel 15 , Tabitha Randell 16 , Fiona J Ryan 17 , Ajay Thankamony 18 , S Faisal Ahmed 19 & Nils P Krone 1,2
1University of Sheffield, Sheffield, United Kingdom. 2Sheffield Children’s Hospital, Sheffield, United Kingdom. 3Leeds General Infirmary, Leeds, United Kingdom. 4Great North Children's Hospital, Newcastle, United Kingdom. 5University of Newcastle, Newcastle, United Kingdom. 6University Hospitals Bristol Foundation Trust, Bristol, United Kingdom. 7Alder Hey Children's Hospital, Liverpool, United Kingdom. 8Great Ormond Street Hospital, London, United Kingdom. 9United Kingdom University of Southampton, Southampton, United Kingdom. 10Centre for Endocrinology, William Harvey Research Institute, London, United Kingdom. 11London and Barts Health NHS Trust, London, United Kingdom. 12Manchester University NHS Foundation Trust, Manchester, United Kingdom. 13Birmingham Women's & Children's Hospital, Birmingham, United Kingdom. 14Faculty of Medicine, National Heart & Lung Institute, Imperial College London, London, United Kingdom. 15Paediatric Endocrine Service, Royal Manchester Children's Hospital, Manchester University NHS Foundation Trust, Manchester, United Kingdom. 16Nottingham Children’s Hospital, Nottingham, United Kingdom. 17Oxford Children's Hospital, Oxford University Hospitals NHS Foundation Trust, Oxford, United Kingdom. 18University of Cambridge, Cambridge, United Kingdom. 19Developmental Endocrinology Research Group, University of Glasgow, Glasgow, United Kingdom
Introduction: Patients with Congenital adrenal hyperplasia (CAH) have increased prevalence of obesity and metabolic problems. The underlining mechanisms are not clearly known. Adipokines are likely involved in this association, however, their role in it is not completely understood.
Objective: We studied adiponectin and leptin in children and young persons with CAH, in relation to their body mass, treatment, hormonal and metabolic biomarkers.
Methods: We analysed a national cohort of 102 patients with 21-hydroxylase deficiency (54 females, age 13.0±2.92 years) recruited between 2016–2019, from 13 centres in the United Kingdom, and 83 sex- and age-matched controls. We collected and analysed anthropometric measurements, data on hormone replacement, and blood samples for biochemical analysis, including an extended steroid profile (17-hydroxyprogesterone, androstenedione, testosterone, 11-hydroxyandrostenedione, 11-ketotestosterone), metabolic profiles, adiponectin and leptin. Blood samples were collected between 9:00-11:00, after the morning hydrocortisone dose.
Results: A difference in adipokines between patients and controls was only found for leptin in males (patients > control, P = 0.033). In patients, leptin had a positive relationship with BMI (leptin(ng/dl) = 4810 + 3939 × BMI-SDS, P < 0.01) and waist circumference (rs = 0.38, P < 0.01), similar to controls. Adiponectin decreased significantly with the BMI only in patients (adiponectin(pg/dl) = 98 – 11 × BMI-SDS, P < 0.01). Regression analysis in patients showed that leptin increased with the insulin level and decreased with the morning relative hydrocortisone dose (leptin(ng/dl) = 11846 + 250 × insulin – 1316 × dose, P < 0.01), but not with the total daily glucocorticoid dose. However, the correlation between leptin and insulin, though significant, was weaker in patients (rs = 0.31, P < 0.01) compared to controls (rs = 0.58, P < 0.01). Of the measured plasma androgens, leptin was only found to correlate with testosterone (rs = -0.29, P = 0.01). However, a negative correlation was found between adiponectin and 17-hydroxyprogesterone (rs = -0.34, P < 0.00), androstenedione (rs = -0.34, P < 0.01), testosterone (rs = -0.33, P < 0.01), 11-hydroxyandrostenedione (rs = -0.32, P < 0.01) and 11-ketotestosterone (rs = -0.28, P = 0.01), which was not present in controls.
Conclusion: A suppressive effect of glucocorticoids on leptin may contribute to the weight gain and metabolic problems found in patients with CAH. The consistent association found between high adiponectin and effective androgen suppression indicate its potential use as a marker of metabolic and androgen control in CAH.
Article tools
My recent searches
My recently viewed abstracts
Authors
ESPE Abstracts
© Bioscientifica 2024 |
Privacy policy |
Cookie settings
BiosciAbstracts
Bioscientifica Abstracts is the gateway to a series of products that provide a permanent, citable record of abstracts for biomedical and life science conferences.
Find out more