Dysregulation of iron and copper homeostasis in nonalcoholic fatty liver

Figure 2 Summary of how iron excess and low copper availability may affect whole body glucose and lipid homeostasis. Iron excess may promote insulin resistance in the liver, muscle and adipose tissue. Iron may increase ER and oxidative stress whereas low copper is potentially associated with an impaired antioxidant defence. These factors may result in the propagation of inflammation, fibrogenesis and hepatocarcinogenesis. TNF-α: Tumor necrosis factor-α; ER: Endoplasmatic reticulum; FFA: Free fatty acid; VAT: Visceral adipose tissue; AT: Adipose tissue.