**2. Relationship between NASH/NAFLD and iron metabolism**

Iron is among the essential trace elements for the existence of all living organisms. It is required for numerous metabolic routines, including energy production, DNA synthesis, oxygen transport and innate immunity, also in the expression of other enzymes involved in the oxidation or reduction of biological substrates and in the activation of iron-containing enzymes, such as the cytochrome system in the mitochondria [13]. Because there is no known physiological mechanism for appropriately and efficiently eliminating the 'too much incorporated' iron, even in severe ironoverloaded conditions, a crucial element in maintaining systemic iron homeostasis is effective and harmonised correspondence among cells that use iron (mainly erythroid precursors), absorb iron from the diet (duodenal enterocytes) and store iron (hepatocytes and tissue macrophages). Therefore, when the iron intake exceeds the cellular provisions and storage capabilities are overflowed, iron toxicity due to overloading may easily develop [14]. Thus, iron balance is maintained through steady and urbane regulatory mechanisms.

Recent studies have established the importance of hepcidin in iron homeostasis as a negative regulator of iron release into the bloodstream by duodenal enterocytes and reticuloendothelial macrophages [15]. Excess iron in the liver promotes steatohepatitis, liver fibrosis, cirrhosis and hepatocellular carcinoma [16]. The discovery of hepcidin and the elucidation of its role in iron metabolism made it possible to develop novel therapies for hemochromatosis, anaemia of inflammation and other ironrelated disorders such as NAFLD/NASH [17]. Hepcidin has a distinct and essential
