Hepcidin Levels and Iron Status in Obese Children and Adolescents: A Case-Control Study in Relation to Leptin and Inflammatory Markers

Abstract

Background: Pediatric obesity is frequently accompanied by low-grade chronic inflammation that can disrupt iron homeostasis. Hepcidin, the key regulator of systemic iron metabolism, rises in inflammatory states and may contribute to obesity-related hypoferremia by reducing intestinal iron absorption and limiting iron release from macrophages. Leptin, an adipokine that increases with adiposity, may further stimulate hepcidin expression, supporting a potential leptin–hepcidin pathway linking obesity to altered iron availability. Objectives: To compare serum hepcidin levels between obese children and adolescents and healthy controls and to characterize accompanying differences in iron-status indicators, leptin, and inflammatory markers. Methods: This single-center case–control study included 33 children and adolescents with obesity and 20 healthy controls from the same hospital-based outpatient catchment area. Obesity was defined using pediatric Body Mass Index (BMI)-for-age percentile criteria (> 95th percentile for age and sex). Complete blood count, serum iron, total iron-binding capacity (TIBC), transferrin saturation (TSAT), ferritin, C-reactive protein (CRP), leptin, and hepcidin were measured. Analyses were performed on an available-case basis without imputation, and between-group comparisons used parametric or non-parametric tests according to data distribution. Results: The obese group had significantly higher anthropometric measures, including height, weight, BMI, and waist circumference (all P < 0.05), while mean age did not differ significantly between groups. Markers of inflammation were higher in obesity (CRP, P = 0.001; white blood cell count, P < 0.001). Leptin concentrations were markedly elevated in obese participants (P < 0.001). Serum hepcidin was also higher in the obese group (28.68 ± 6.64 vs. 22.51 ± 8.52 ng/mL; P = 0.035). Serum iron and TSAT tended to be lower in obesity but did not reach statistical significance, whereas TIBC was significantly higher in obese participants (P = 0.036). Hemoglobin and ferritin did not differ significantly between groups. Conclusions: Obese children and adolescents exhibited higher hepcidin and leptin levels together with inflammatory findings, supporting the concept that pediatric obesity may influence iron regulation through inflammatory and adipokine-related pathways. The pattern of higher TIBC with only a trend toward lower serum iron/TSAT may be compatible with early impairment of iron availability; however, these findings should not be interpreted as definitive iron deficiency in the absence of prespecified diagnostic thresholds and adjustment for potential confounders.