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Vitamin B12 from food sources is bound to proteins and is only released by an adequate concentration of hydrochloric acid in the stomach. Free vitamin B12 is then immediately bound to glycoproteins originating from the stomach and salivary glands. This glycoprotein complex protects vitamin B12 from chemical denaturation. Gastrointestinal absorption of vitamin B12 occurs in the small intestine by an active process requiring the presence of intrinsic factor, another glycoprotein, which the gastric parietal cells secrete after being stimulated by food. The absorption of physiological doses of vitamin B12 is limited to approximately 10µg/dose. The vitamin B12 intrinsic factor complex is then absorbed through phagocytosis by specific ileal receptors. Once absorbed, the vitamin is transferred to a plasma-transport protein which delivers the vitamin to target cells. A lack of intrinsic factor results in malabsorption of cobalamin. If this is untreated, potentially irreversible neurological damage and life-threatening anaemia develops (see deficiency).

Regardless of dose, approximately 1% of vitamin B12 is absorbed by passive diffusion, so this process becomes quantitatively important at pharmacological levels of exposure. Once absorbed, vitamin B12 is stored principally (60%) in the liver. The average B12 content is approximately 1.0 mg in healthy adults, with 20-30 µg found in the kidneys, heart, spleen and brain. Estimates of total vitamin B12 body content for adults range from 0.6 to 3.9 mg with mean values of 2-3 mg. The normal range of vitamin B12 plasma concentrations is 150-750 pg/ml, with peak levels achieved 8-12 hours after ingestion.

Excretion of vitamin B12 is proportional to stores and occurs mainly by urinary and faecal routes. Vitamin B12 is very efficiently conserved by the body, with 65-75% re-absorption in the ileum of the 0.5-5 µg excreted into the alimentary tract per day (mainly into the bile). This helps to explain the slow development (over several years) of deficiency states in subjects with negligible vitamin B12 intake, such as vegans. Subjects with a reduced ability to absorb cobalamin via the intestine (lack of intrinsic factor) develop a deficiency state more rapidly.

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