Didem HELVACIOĞLU, Barış YILMAZ, Abdullah BEREKET
The Journal of Pediatric Research - 2026;13(1):58-64
Aim: Obesity and iron deficiency represent two of the most prevalent nutritional disorders worldwide. Obesity is accompanied by chronic low-grade inflammation, with elevated circulating levels of pro-inflammatory cytokines, particularly interleukin 6 (IL-6). Obesity-related inflammatory pathways promote hepatic hepcidin synthesis, with IL-6 serving as a central mediator of hepcidin transcription under inflammatory conditions. Hepcidin is the principal regulator of intestinal iron absorption, and its increased expression contributes to impaired iron availability in obese individuals. This study aimed to examine the association between obesity and iron deficiency and to clarify the role of hepcidin in iron homeostasis among obese children. Materials and Methods: This case-control study enrolled 50 children with obesity [body mass index (BMI) >95th percentile] and 50 healthy non-obese children (BMI between the 5th and 95th percentiles), aged 8-18 years. The evaluated parameters included hemoglobin (Hb), mean corpuscular volume (MCV), serum iron, ferritin, total iron-binding capacity, transferrin saturation (TS), as well as serum hepcidin and IL-6 levels. Results: Obese children had significantly lower serum iron, Hb, MCV, ferritin, and TS (all p<0.05), and higher hepcidin and IL-6 levels (p=0.024 and p=0.032, respectively), compared to the controls. Hepcidin levels were directly correlated with IL-6 (p<0.001) and BMI standard deviation scores (p=0.019). Inverse correlations were observed between hepcidin and iron (p=0.024), hepcidin and Hb (p=0.001), and hepcidin and MCV (p=0.02). Conclusion: Chronic inflammation of obesity and elevated hepcidin levels result in the low iron states in obese children.
