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. 2018 Sep 26;7(10):304. doi: 10.3390/jcm7100304

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© 2018 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Structure and metabolism of the vitamin B12, with a focus on gastrointestinal disorders responsible for vitamin B12 deficiency. The digestive step of the metabolic of cobalamin (cbl) begins with nutrient intake to its intestinal absorption. Endocytic receptors and proteins responsible for vitamin B12 intestinal absorption include cubilin (CUBN), amnionless (AMN), receptor-associated protein and megalin (MGA1). The membrane megalin/transcobalamin II (TCII)-receptor complex allows the cellular uptake of cbl. Lysosomal-mediated degradation of TCII and subsequent release of free-cbl is essential for vitamin B12 metabolic functions. MS, methonine synthase; THF, tetrahydrofolate; MTHFR, methylene tetrahydrofolate reductase; MCM, methylmalonyl CoA mutase.