HepcidinSekretion

Hepcidin secretion refers to the regulated release of the peptide hormone hepcidin into the bloodstream, playing a critical role in iron homeostasis. Hepcidin is primarily synthesized and secreted by hepatocytes, the liver cells, and acts as a key regulator of iron absorption and distribution within the body. Its primary function is to control iron levels by binding to ferroportin, a protein that facilitates iron export from cells into the bloodstream. When hepcidin levels rise, ferroportin is internalized and degraded, reducing iron release from enterocytes in the intestine and macrophages, thereby limiting iron absorption and storage.

The secretion of hepcidin is tightly controlled by various physiological signals, including body iron stores, inflammation, and erythropoietic activity. Elevated iron levels in the liver stimulate hepcidin production through the bone morphogenetic protein (BMP) and hepcidin amplifier (HAMP) signaling pathways, ensuring iron is retained when sufficient stores are present. Conversely, low iron levels suppress hepcidin secretion, allowing increased iron absorption to replenish stores.

Inflammatory responses also influence hepcidin secretion, as cytokines such as interleukin-6 (IL-6) can induce its production, contributing to the anemia of chronic disease by restricting iron availability for erythropoiesis. Additionally, erythropoietic activity, particularly during red blood cell production, suppresses hepcidin expression to ensure adequate iron supply for hemoglobin synthesis.

Disruptions in hepcidin secretion can lead to iron-related disorders. For example, mutations causing low hepcidin levels result in hereditary hemochromatosis, characterized by excessive iron absorption and accumulation. Conversely, conditions associated with elevated hepcidin, such as inflammation or certain genetic disorders, may cause iron-restricted anemia. Understanding hepcidin secretion is essential for diagnosing and managing iron metabolism disorders.