The impact of childhood obesity on iron deficiency and its relationship with hepcidin, leptin, interleukin-6

Objective: The relationship between iron deficiency, and obesity has been shown in recent years. The reason is thought to be the anemia of chronic disease caused by chronic inflammation originating from adipose tissue. Our aim is to determine the relationship between obesity and iron deficiency, the place of hepcidin in iron homeostasis, and inflammation occurring in obesity, and also demonstrate its effect of the parametres of iron metabolism in obese children. Methods: This study was performed with 54 obese (body mass index (BMI)>95p) and 51 normal weighted (BMI: 5-95p) children aged between 5-16 years. In two groups serum iron, total iron binding capacity (TIBC), ferritin, hemoglobin, transferrin saturation index (TSI), interleukin-6 (IL-6), C-reactive protein (CRP), leptin and hepcidin were studied. Results: When compared with the control group; decreased serum iron (p=0.004), hemoglobin (Hb) (p=0.010), TSI (p=0.001), increased hepcidin (p=0.001), TDBK (p=0.041), leptin (p=0.001), CRP (p=0.001) levels were found in obese children. In 18 cases (%33.3) decreased levels of Hb were detected, while in 8 of these cases (% 14.8) the parameters were found compatible with iron deficiency anemia (IDA). Five cases (% 9.2) were accepted as anemia of chronic disease. In the obese group the number of patients with IDA was found statistically significantly higher (p=0.032). Besides higher BMI (p=0.001), however decreased hepcidin (p=0.008), and ferritin (p=0.006) levels were detected in anemia patients. Conclusion: In our study obesity was found to be associated with iron deficiency. The effect of hepcidin was shown to be the cause of iron deficiency. Every study to be performed in order to understand the relationship between inflammation, obesity and erythropoiesis will contribute to the development of nutritional, and/or pharmacological therapies with the aim to prevent the onset of iron deficiency in obese patients.