Iron Metabolism is the essential, tightly regulated physiological process governing the absorption, transport, storage, and utilization of iron within the human body. This trace element is indispensable for fundamental biological processes, most notably oxygen transport via hemoglobin, cellular respiration through the electron transport chain, and DNA synthesis. Clinical assessment of iron metabolism, including ferritin and transferrin saturation, is vital for diagnosing conditions ranging from anemia due to deficiency to hemochromatosis due to overload, both of which severely impact systemic health.
Origin
The term combines the element “iron,” derived from the Old English īsern, with “metabolism,” from the Greek metabolē, meaning “change.” The understanding of this complex process is ancient, tied to early recognition of blood-related disorders, but the intricate molecular details, including the roles of transferrin and hepcidin, were elucidated in modern biochemistry. The clinical focus on its metabolism reflects the dual risk of both deficiency and toxicity.
Mechanism
The regulation of iron levels is centrally controlled by the peptide hormone hepcidin, which is produced in the liver and acts as the master regulator of iron entry into the plasma. Hepcidin controls the degradation of ferroportin, the only known cellular iron exporter, thereby regulating absorption from the gut and release from storage sites like macrophages and hepatocytes. This precise hormonal mechanism ensures that iron levels are maintained within a narrow therapeutic window, preventing both functional iron deficiency and toxic accumulation.
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