Nutrition Essentials: Vitamins and Iron

High hepcidin levels inhibit iron absorption by binding to ferroportin, a protein that transports iron out of cells. This blocks iron release from enterocytes and macrophages, reducing iron absorption.

Hepcidin, a protein, binds to ferroportin, the iron transporter. This binding prevents iron from leaving cells, leading to reduced intestinal iron absorption and decreased iron release from macrophages.

Intestinal cells (enterocytes) absorb iron. High hepcidin levels decrease absorption by reducing the release of iron from enterocytes.

Macrophages recycle iron. High hepcidin levels inhibit iron release from macrophages, reducing overall iron absorption.

High hepcidin levels decrease the activity of the protein DMT1, which is involved in iron absorption in the gut. This leads to reduced iron absorption.

Intestinal cells (enterocytes) live for only 3-4 days.

Iron leaving enterocytes (through the basolateral border) is transported in the body, which needs oxidation to enter the bloodstream(ferrioxidase enzyme). Iron then binds to transferrin (a transport protein).

Hepcidin is a major regulator of iron absorption.

Proteins are absorbed from the terminal ileum through pinocytosis, requiring trypsin from the pancreas for the process. The absorbed protein enters the bloodstream, binding to transcobalamin II; excess is stored in the liver.

Iron is primarily stored in the body as ferritin (main storage form), with hemosiderin being aggregated ferritin molecules. Storage locations include liver, spleen, enterocytes, and bone marrow. Small amounts of iron are found in plasma, bound to transferrin.

Adults require approximately 30mg of iron daily. This is primarily from the recycling of hemoglobin breakdown in the liver and spleen. Males lose roughly 0.5 – 1.0 mg daily, while females lose approximately twice that amount due to menstruation.

Dietary iron comes in two forms: heme iron (mainly from meat) and non-heme iron (from plants). Heme iron is more bioavailable (easier to absorb) than non-heme iron.

Free iron in the body is a toxic substance as it leads to the production of reactive oxygen species (ROS).

A major regulator of iron absorption and release by macrophages.

Hepcidin degrades ferroportin, inhibiting intestinal iron absorption, and the release of iron from macrophages and the liver.

Low oxygen levels (hypoxia) and erythropoietin (stimulates red blood cell production) decrease hepcidin secretion, allowing for increased iron absorption for red blood cell production.

High iron levels in the body increase hepcidin secretion to maintain iron homeostasis.

Inflammation increases hepcidin secretion, which can lead to anemia.

A genetic mutation causing increased iron absorption.

Blood removal (phlebotomy) to reduce excess iron.

Iron chelating agents to remove excess iron.

Excess hemosiderin (iron storage protein) in tissues.

Skin pigmentation, pancreatic damage (diabetes), liver cirrhosis, and hepatic carcinoma.

Mean corpuscular hemoglobin; average amount of hemoglobin per red blood cell.

Mean corpuscular volume; average volume of a red blood cell.

Mean corpuscular hemoglobin concentration; average concentration of hemoglobin in a red blood cell.

A mutation in the Ab gene that can lead to sickle cell anemia.

Blockage of small blood vessels.

Anemia with normal red blood cell size and hemoglobin.

Anemia with small, pale red blood cells.

Anemia with large red blood cells.

Anemia caused by low iron intake or absorption.

Anemia due to lack of vitamin B12, often from absorption issues.

Anemia caused by rapid blood loss.

Anemia from bone marrow depression.

Anemia associated with chronic inflammation or disease.