Eur J Pediatr 2014 Jul;173(7):947-51

Serum hepcidin levels and iron metabolism in obese children with and without fatty liver: case-control study.

Demircioğlu F1, Görünmez G, Dağıstan E, Göksügür SB, Bekdaş M, Tosun M, Kızıldağ B, Kısmet E.
Hepcidin is a regulator of iron balance that is increased in obesity. It reduces the absorption of iron, reduces the transfer of iron from macrophages to the plasma and/or prevents mobilisation of stored iron. Obese patients with non-alcoholic fatty liver disease (NAFLD) demonstrate adipokine and cytokine release promoting inflammatory response. We aimed to analyse the hepcidin levels and iron metabolism in obese children with and without NAFLD and non-obese healthy controls. The study population consisted of 110 children aged 7-18 years in three groups: 50 obese patients without NAFLD, 30 obese patients with NAFLD, and 30 non-obese healthy controls. Serum hepcidin, ferritin, and iron levels, iron-binding capacity, lipid profile, and liver function tests were measured, and hepatic ultrasonography was performed in all participants. Obese patients' white blood cell counts, total cholesterol, triglyceride levels, and homeostatic model assessment of insulin resistance (HOMA-IR) were significantly higher than those of the control group. Iron-binding capacity was significantly higher in obese patients without NAFLD compared with obese patients with NAFLD (p = 0.002). Hepcidin levels were not significantly different between obese patients and the control group. However, hepcidin levels in obese patients with NAFLD were significantly higher than those in obese patients without NAFLD (p < 0.001).
l="UNLABELLED">Hepcidin is a regulator of iron balance that is increased in obesity. It reduces the absorption of iron, reduces the transfer of iron from macrophages to the plasma and/or prevents mobilisation of stored iron. Obese patients with non-alcoholic fatty liver disease (NAFLD) demonstrate adipokine and cytokine release promoting inflammatory response. We aimed to analyse the hepcidin levels and iron metabolism in obese children with and without NAFLD and non-obese healthy controls. The study population consisted of 110 children aged 7-18 years in three groups: 50 obese patients without NAFLD, 30 obese patients with NAFLD, and 30 non-obese healthy controls. Serum hepcidin, ferritin, and iron levels, iron-binding capacity, lipid profile, and liver function tests were measured, and hepatic ultrasonography was performed in all participants. Obese patients' white blood cell counts, total cholesterol, triglyceride levels, and homeostatic model assessment of insulin resistance (HOMA-IR) were significantly higher than those of the control group. Iron-binding capacity was significantly higher in obese patients without NAFLD compared with obese patients with NAFLD (p = 0.002). Hepcidin levels were not significantly different between obese patients and the control group. However, hepcidin levels in obese patients with NAFLD were significantly higher than those in obese patients without NAFLD (p < 0.001).

CONCLUSIONS:

Hepcidin levels were significantly higher in obese children with NAFLD than those without NAFLD. Obese children with NAFLD should receive attention regarding iron metabolism disorders. Serum hepcidin could be a marker of iron metabolism status and NAFLD in these groups of patients.