Hepcidin, ferritin, and transferrin are among the several proteins that are mostly found in the liver and are involved in the control of iron metabolism. These proteins play a part in iron metabolism and are acute-phase reactants whose expression can change in response to inflammation or hepatic or systemic damage. Pro-inflammatory mediators generated by macrophages, which contribute to the development of peripheral insulin resistance, may have an impact on hepcidin synthesis. Ferroportin-1, the sole known Fe exporter, is bound by circulating hepcidin, which then drives enterocytes and splenic macrophages to internalize and degrade it.

An upward body of data indicates that iron deficiency plays a major role in the emergence of a number of several disorders. Hepcidin and systemic iron homeostasis play a significant role in liver disorders and type-2 diabetes. These include erythropoiesis, infection, inflammation, body iron storage, and plasma iron content. The mechanism and regulation of hepcidin-induced iron overload, as well as associated liver and diabetic disorders, are summed up in this review. Additionally, we outline examples of associations between hepcidin and blood iron levels in a range of metabolic diseases, primarily liver and diabetes.