Leptin and adiponectin in children and young persons with congenital adrenal hyperplasia
Author(s)
Type
Journal Article
Abstract
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.
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.
Date Issued
2025-09-01
Date Acceptance
2025-08-06
Citation
European Journal of Endocrinology, 2025, 193 (3), pp.329-339
ISSN
0804-4643
Publisher
Oxford University Press (OUP)
Start Page
329
End Page
339
Journal / Book Title
European Journal of Endocrinology
Volume
193
Issue
3
Copyright Statement
© The Author(s) 2025. Published by Oxford University Press on behalf of European Society of Endocrinology. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.
License URL
Identifier
https://www.ncbi.nlm.nih.gov/pubmed/40795401
PII: 8228636
Subjects
adiponectin
androgens
congenital adrenal hyperplasia
glucocorticoid treatment
leptin
Humans
Adrenal Hyperplasia, Congenital
Leptin
Female
Male
Adiponectin
Adolescent
Child
Body Mass Index
Hydrocortisone
Glucocorticoids
Case-Control Studies
Biomarkers
Publication Status
Published
Coverage Spatial
England
Article Number
lvaf165
Date Publish Online
2025-08-08