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Talk:Haptocorrin

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any more information? Like what makes haptocorrin?

Believe there is sufficient evidence that around 1% of B12 is passively absorbed from the GI, even without intrinsic factor. This is the basis for treating malabsorption disorders with oral supplements. Would appreciate if author could please update this wiki. Certainly 'active' absorption (~30-60% of GI cobalamin) is not possible in the absence of IF. — Preceding unsigned comment added by 203.48.242.193 (talk) 06:29, 31 August 2012 (UTC)[reply]

Function

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Under Function, the phrase "a MW of 45,000 dalton" needs to be explained, and "MW" and "dalton" need in-text definitions and links, if available. The article is meant for non-experts who will be unfamiliar with these terms. The rest of the article is admirably comprehensible to all.

Also, if MW is pronounced "em-double-you," the phrase should read "an MW." KC 07:33, 14 April 2016 (UTC)

Thanks. KC 07:33, 14 April 2016 (UTC) — Preceding unsigned comment added by Boydstra (talkcontribs)

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Most descriptions indicate that the gastric intrinsic factor (encoded by GIF) protects B12 in the stomach and carries it into the blood and cells. Where is the source for transcobalamin-1 being secreted by the salivery glands? In the cells, the B12 disassociates and attaches to transcobalamin-1 (or other intrinsic factors). The transcobalamin-1 - B12 complex can also be transported to the liver where excess B12 can be stored (it didn't say how).

LDCorey (talk) 22:37, 6 November 2019 (UTC)[reply]

question

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is it possible to be deficient in haptocorrin? and is it possible to have autoantibodies to haptocorrin? if so, could that condition be considered (perhaps mistakenly) as pernicious or megaloblastic anemia?````