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[[Intracellular]] vitamin B12 is maintained in two active coenzymes, methylcobalamin and 5-deoxyadenosylcobalamin. In the face of vitamin B12 deficiency, conversion of methylmalonyl-CoA to [[succinyl-CoA]] cannot take place, which results in accumulation of methylmalonyl-CoA and aberrant fatty acid synthesis. In the other enzymatic reaction, methylcobalamin supports the methionine synthase reaction, which is essential for normal metabolism of folate. The folate-cobalamin interaction is pivotal for normal synthesis of [[purines]] and [[pyrimidines]] and the transfer of the methyl group to cobalamin is essential for the adequate supply of [[tetrahydrofolate]], the substrate for metabolic steps that require folate. In a state of vitamin B12 deficiency, the cell responds by redirecting folate metabolic pathways to supply increasing amounts of [[levomefolic acid|methyltetrahydrofolate]]. The resulting elevated concentrations of [[homocysteine]] and [[methylmalonic acid|MMA]] are often found in patients with low serum vitamin B12 and can usually be lowered with successful vitamin B12 replacement therapy. However, elevated [[methylmalonic acid|MMA]] and [[homocysteine]] concentrations may persist in patients with cobalamin concentrations between 200 and 350 pg/mL. Supplementation with vitamin B12 during conditions of deficiency restores the intracellular level of cobalamin and maintains a sufficient level of the two active coenzymes: methylcobalamin and deoxyadenosylcobalamin.

Translations:Hydroxocobalamin/19/en - Revision history

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