Duodenum Information and Courses from MediaLab, Inc.
These are the MediaLab courses that cover Duodenum and links to relevant pages within the course.
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Bilirubin is a degradation product of hemoglobin. When red blood cells (RBCs) have reached the end of their normal life span (approximately 120 days), they are destroyed in the spleen and liver. Hemoglobin that is freed in the process is further broken down into iron, protein, and protoporphyrin. Protoporphyrin is converted to bilirubin and released into the circulation. Bilirubin binds to albumin and is transported in the blood to the liver. This unconjugated bilirubin is insoluble in water and cannot be filtered through the glomerulus of the kidney. Bilirubin is then conjugated with glucuronic acid in the liver. This conjugated bilirubin is water soluble and is excreted by the liver through the bile ducts and into the duodenum; bilirubin does not normally appear in the urine. However, if the normal degradation cycle is disrupted, as happens with cirrhosis, hepatitis, and other conditions that damage the liver, conjugated bilirubin will appear in the urine. Since conjugated bilirubin is not bound to protein, it is easily filtered through the glomerulus and excreted in the urine whenever the plasma bilirubin level is increased.
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|Iron Intake and Recycling|
The typical daily diet of most Americans contains approximately 10 to 15 mg of iron. Sources of dietary iron include heme iron from meats and nonheme iron from whole grains and vegetables. Many processed foods, such as breakfast cereal, are fortified with iron. However, the normal individual absorbs only 5% to 15% of dietary iron, or about 1 to 2 mg daily. Females may absorb slightly more iron than males as they require more iron to replace that lost through menstruation and to meet the increased need for iron in pregnancy.Absorption of iron occurs through the mucosal cells in the duodenum (proximal small intestine). Dietary iron that is not absorbed is excreted in the feces. Intestinal absorption provides the means for regulating the amount of iron in the body.The amount of Iron absorbed is normally low because iron is well conserved within the body. Heme iron from senescent erythrocytes is cycled back into the iron pool and reused for incorporation into developing erythrocytes. Furthermore, iron is normally lost from the body only in very small amounts, primarily through desquamation of mucosal cells in the gastrointestinal tract and losses through body secretions, including urine, sweat and feces. Therefore, under normal conditions, very little dietary iron needs to be absorbed to maintain iron homeostasis.(3)
|Regulation of Iron Equilibrium|
Regulation of iron equilibrium occurs mainly through the process of absorption. Iron is absorbed through the mucosal cells lining the duodenum. A variety of proteins are involved in this process. Hepcidin, an antimicrobial protein primarily produced in the liver, has been recently found to be a major (negative) regulator of dietary iron absorption by disrupting cellular iron transport in the intestine. Decreased levels of hepcidin are related to increased iron absorption into the bloodstream. Hepcidin is increased in response to iron overload and inflammation. (4)Additional proteins involved in iron metabolism include transferrin (Tf), transferrin receptor (TfR), ferroportin, HFE protein, hemojuvelin, and others. Their roles in iron absorption are complex and in some instances incompletely understood.Factors affecting iron absorption include: Tissue stores, e.g., decreased stored iron is associated with a decrease in hepcidin and increase in iron absorption. Rate of hematopoietic activity, e.g., an increased rate of erythropoiesis is associated with a decrease in hepcidin and an increase in iron absorption. Oxygen concentration in tissues, e.g., hypoxia decreases hepcidin and increases iron absorption, thereby promoting increased erythopoiesis. Dietary intake, including form of iron ingested, e.g., heme iron is more readily absorbed than non-heme forms of iron. Condition of GI tract mucosal cells Intraluminal factors, e.g. intestinal motility
Once absorbed through the mucosal cells of the duodenum, iron is bound to a carrier plasma protein, transferrin (Tf), for movement to sites of utilization. Almost all iron in plasma is bound to Tf, and most Tf-bound iron is carried to the bone marrow to be incorporated into developing erythrocytes. Transferrin is normally about 20% to 40% saturated with iron. (5)Transferrin releases iron to specific transferrin receptors (TfRs) for movement into cells. Transferrin receptors are found on all cells, but are found in relatively high concentration in erythroid precursors, hepatocytes, and placental cells. When the capacity of plasma Tf to bind iron is exceeded, i.e., transferrin saturation (TS) is higher than normal, excess iron is taken up by hepatocytes and other cells. A brief summary of iron metabolism is illustrated.
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