*Regulation of Iron Metabolism in NAFLD/NASH DOI: http://dx.doi.org/10.5772/intechopen.107221*

Moreover, these results tend to suggest that the link between hyperferritinemia and NAFLD could be explained by insulin resistance. In NAFLD pathogenesis, the role of hepatic iron has largely focused on the generation of oxidative stress by iron. Considering oxidative stress is an established key component of NASH pathogenesis [107], the role of iron mediating liver injury in NAFLD via this mechanism has been well studied. Oxidative stress leads to cell death via depletion of ATP, NAD and glutathione, and by direct damage to DNA, lipids and proteins within hepatocytes in NASH. Furthermore, oxidative stress leads to an increase in the production of pro-inflammatory cytokines and fibrogenic responses. Not only does oxidative stress potentiate steatohepatitis, characterised by inflammation and cell death, but it can also increase steatosis by preventing the secretion of very low-density lipoprotein (VLDL) through increased degradation of apolipoprotein B100 (ApoB100) [108].

In conclusion, iron has been gradually recognised as a regulator of adipose tissue function. There are definite pieces of evidence which support the role of iron in the regulation of adipose tissue inflammation, adipokine regulation and adipose tissue lipolysis. At present, most pieces of evidence support the role of adipose tissue iron in the pathogenesis of insulin resistance and T2DM, although clearly, these mechanisms may be highly relevant in NAFLD.

It has been suggested that elevated serum ferritin is associated with several metabolic disorders. However, no reported study has assessed the association between serum ferritin and sarcopenia despite the close relationship between sarcopenia and metabolic disorders.

The question then arises whether the concentration of hepcidin in T2DM subjects is primary or secondary to elevated body iron stores. This might be an important assignment to find a key to the settlement of the dispute.
