Ferrop2t Fee Liver
Macropnage
Biooa
Hephaestin Plasma
° veanstorin
Must be Fe®*
to reabsoro
Corulopiasmin
Enytroid
Lost by shedding
of epithelial cels
‘Sensor
LTranstetin ion (oss ron attached to tranetertin
‘Ttranserption of epcicin > J nepcicin => * iron
eabsorption in uodenum and release of on rom
macrophages: “Transterin receptor
{TTranstertin ito (more ron attached to transfer: Transterrin with Fo?
‘7 Transerption of hepeidin > T hepclain “> «ron
reabsorpion in duodenum and release of Fon rom
macrophages.
12.8: iron absorption. The reabsorption of iron is dependent on total iron stores in the body, which i reflected
in the amount of iron that iz bound to transferrin. Transferrin with iron binds to immature precursor cells of
Normal enterocytes, which serve as ron sensors in the duodenum. The HFE hemochromatosis gene (HFE gene)
Protein product in these sensor cels acting together with the transferrin receptor causes the precursor cells 0
Gifferentiate into mature enterocytes that can actively reabsorb iron. Absorptvely active enterocytes absorb
‘ferrous iron (Fe") directly via heme carrier protein 1 or through the divalent metal transporter (OMT), Absorbed
itan i ether stored in the cytoplasm as mucosal ferritin or Wansferred to the ferroporin 1 port where itis con
verted to ferric iron (Fe") by hephaestin and ceruloplasmin. Plasma transferrin then binds the iron and carries it
‘0 erythroid precursors in the bane marrow. The HFE protein also regulates the production of another protein