Body of iron
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Body Iron: Metabolism, Assessment, and Health Implications
Iron Metabolism and Regulation
Iron is a crucial element for various biological processes, primarily bound to hemoglobin in red blood cells. The body recycles iron from old red blood cells through macrophages in the spleen, liver, and bone marrow. Dietary iron is absorbed in the intestines and transported to the bloodstream, where it binds to transferrin and is distributed to various cells. The liver plays a significant role in iron storage, primarily in the form of ferritin. Hepcidin, a hormone produced by the liver, regulates iron levels by controlling the degradation of ferroportin, the iron transporter, thus modulating iron release into the blood.
Quantitative Assessment of Body Iron
Accurate assessment of body iron is essential for diagnosing and managing iron-related disorders. One method involves measuring the ratio of serum transferrin receptor to serum ferritin, providing a reliable estimate of body iron stores. This method has shown a normal distribution of body iron in different populations, such as US men and pregnant Jamaican women. Additionally, this approach has been useful in evaluating iron absorption in supplementation trials. Transferrin saturation (TSAT) is another important biomarker, reflecting the balance between plasma iron and its transport protein, transferrin. TSAT is widely used in clinical practice to detect iron deficiency or overload, although it has limitations, especially in inflammatory conditions.
Iron Deficiency and Iron Overload
Iron deficiency, affecting over 1.2 billion people globally, can result from increased physiological needs, reduced intake, defective absorption, or chronic blood loss. The body adapts to iron deficiency by increasing iron uptake and retention through regulatory proteins and suppressing hepcidin to enhance iron release from enterocytes and macrophages. Conversely, iron overload, often due to hereditary factors or repeated transfusions, leads to organ dysfunction through the production of reactive oxygen species. Advanced iron overload can cause liver and heart failure, as well as endocrine dysfunctions.
Body Iron and Type 2 Diabetes Risk
Emerging evidence suggests a link between body iron stores, dietary heme-iron intake, and the risk of type 2 diabetes (T2D). Meta-analyses have shown that higher ferritin levels and increased heme-iron intake are associated with a greater risk of T2D. Specifically, individuals with the highest ferritin levels had a significantly higher relative risk (RR) of developing T2D compared to those with the lowest levels . Similarly, high heme-iron intake was associated with an increased risk of T2D, while no significant association was found with total iron, non-heme iron, or supplemental iron intake.
Iron Excretion and Loss
Iron excretion in humans is minimal, with daily losses occurring through desquamated mucosal cells, blood, bile, urine, and skin. Studies have shown that daily iron losses vary among different populations, with higher losses observed in groups with greater iron stores. These findings highlight the body's limited capacity to excrete iron, emphasizing the importance of regulating iron intake and storage to prevent overload.
Conclusion
Understanding body iron metabolism, accurate assessment methods, and the health implications of iron deficiency and overload is crucial for managing iron-related disorders. The association between body iron stores and the risk of type 2 diabetes underscores the need for careful monitoring of iron levels, particularly in populations at risk for metabolic diseases. Advances in diagnostic techniques and personalized therapeutic approaches will continue to improve the management of iron status and related health outcomes.
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