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| align="center" colspan="2" |
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| colspan="2" bgcolor="#dddddd" | Identifiers
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| bgcolor="#e7dcc3" | Symbol(s)
| bgcolor="#eeeeee" | [GIF]
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| bgcolor="#e7dcc3" | Entrez
| bgcolor="#eeeeee" | [2694]
|- class="hiddenStructure"
| bgcolor="#e7dcc3" | OMIM
| bgcolor="#eeeeee" | [609342]
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| bgcolor="#e7dcc3" | RefSeq
| bgcolor="#eeeeee" | [NM_005142]
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| bgcolor="#e7dcc3" | UniProt
| bgcolor="#eeeeee" | [P27352]
|- class="hiddenStructure"
| bgcolor="#e7dcc3" | PDB
| bgcolor="#eeeeee" | []
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| colspan="2" bgcolor="#dddddd" | Other data
|- class="hiddenStructure"
| bgcolor="#e7dcc3" | EC number
| bgcolor="#eeeeee" | []
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| bgcolor="#e7dcc3" | Locus
| bgcolor="#eeeeee" | Chr. 11[q13]
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|}
Intrinsic factor is a glycoprotein produced by the parietal cells of the stomach. It is necessary for the absorption of vitamin B{{ssub later on in the small intestine.
Upon entry into the stomach, vitamin B12 becomes bound to one of two B12 binding proteins present in gastric juice. In the less acidic environment of the small intestine, these proteins dissociate from the vitamin, enabling it to bind to intrinsic factor and enter the portal circulation through a receptor in the ilealmucosa specific for the B12-intrinsic factor complex.
In pernicious anemia, an autoimmune disease, autoantibodies directed against intrinsic factor or parietal cells themselves lead to an intrinsic factor deficiency, malabsorption of vitamin B12, and subsequent megaloblastic anemia. Atrophic gastritis can also cause intrinsic factor deficiency and anemia through damage to the parietal cells of the stomach wall. Pancreatic exocrine insufficiency can interfere with normal dissociation of vitamin B12 from its binding proteins in the small intestine, preventing its absorption via the intrinsic factor complex.
