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Leptin and adiponectin in children and young persons with congenital adrenal hyperplasia

Lookup NU author(s): Professor Timothy CheethamORCiD

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This work is licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0).


Abstract

© The Author(s) 2025. Published by Oxford University Press on behalf of European Society of Endocrinology.OBJECTIVES: Patients with congenital adrenal hyperplasia (CAH) have increased prevalence of metabolic problems. We studied adiponectin, leptin and resistin in children with CAH, in relation to BMI, treatment, hormonal and metabolic biomarkers. DESIGN AND METHODS: We analysed 101 patients with 21-hydroxylase deficiency (54 females, 13.0 ± 2.92 years) from 13 centres in the United Kingdom, and 83 sex- and age-matched controls. Blood parameters (leptin, adiponectin, resistin, metabolic and hormonal markers) were measured in fasted state, between 09:00 and 11:00, after the first glucocorticoid (GC) dose. RESULTS: A difference in adipokines between patients and controls was only found for leptin in males (patients > control, P = .033). In patients and controls, leptin had a positive relationship with BMI-SDS (P < .001). However, adiponectin decreased with the BMI only in patients (P < .001). Contrary to published evidence on the effect of synthetic steroids on leptin, in our cohort, leptin decreased with the increasing first daily hydrocortisone (HC) dose (Log10Leptin = 4.1- 0.08xfirstGCdose (mg/m2), P = .009) but not with the total daily dose. When correcting for BMI, a positive relationship between leptin and insulin was only found in controls (P < .001). Adiponectin decreased with steroid precursor and androgen concentrations (17-hydroxyprogesterone, androstenedione, testosterone, 11-hydroxyandrostenedione, 11-ketotestosterone) in patients. CONCLUSION: Our findings indicate a decrease in leptin with the HC dose, consistent with a detrimental effect of glucocorticoid on satiety and hunger pathways in CAH. Adiponectin was decreased in patients with increased androgens concentrations, suggesting it may be used as an indicator of metabolic risk associated with poor hormonal CAH control.


Publication metadata

Author(s): Bacila IA, Lawrence NR, Alvi S, Cheetham TD, Crowne E, Das U, Dattani MT, Davies JH, Gevers E, Keevil B, Krone RE, Lawrie A, Patel L, Randell T, Ryan FJ, Ahmed SF, Krone NP

Publication type: Article

Publication status: Published

Journal: European Journal of Endocrinology

Year: 2025

Volume: 193

Issue: 3

Pages: 329-339

Print publication date: 01/09/2025

Online publication date: 08/08/2025

Acceptance date: 06/08/2025

Date deposited: 09/09/2025

ISSN (print): 0804-4643

ISSN (electronic): 1479-683X

Publisher: Oxford University Press

URL: https://doi.org/10.1093/ejendo/lvaf165

DOI: 10.1093/ejendo/lvaf165

Data Access Statement: The datasets generated and analysed in this study are not publicly available but are available from the corresponding author on reasonable request

PubMed id: 40795401


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Funding

Funder referenceFunder name
British Heart Foundation FS/18/52/33808
Diurnal Ltd.
National Institute of Health and Care Research

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