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Absorption and metabolism of vitamin C
There is active transport of the vitamin at the intestinal mucosal brush border membrane. Both ascorbate and dehydroascorbate are absorbed across the buccal mucosa by carrier-mediated passive processes. Intestinal absorption of dehydroascorbate is carrier mediated, followed by reduction to ascorbate before transport across the basolateral membrane.
Some 80–95% of dietary ascorbate is absorbed at usual intakes (up to about 100 mg/day). The frac-tional absorption of larger amounts of the vitamin is lower, and unabsorbed ascorbate from very high doses is a substrate for intestinal bacterial meta-bolism, causing gastrointestinal discomfort and diarrhea.
About 70% of blood ascorbate is in plasma and erythrocytes, which do not concentrate the vitamin from plasma. The remainder is in white cells, which have a marked ability to concentrate it.
Both ascorbate and dehydroascorbate circulate in free solution, and also bound to albumin. About 5% of plasma vitamin C is normally dehydroascorbate. Both vitamers are transported into cells by glucose transporters, and concentrations of glucose of the order of those seen in diabetic hyperglycemia inhibit tissue uptake of ascorbate.
There is no specific storage organ for ascorbate; apart from leukocytes (which account for only 10% of total blood ascorbate), the only tissues showing a significant concentration of the vitamin are the adrenal and pituitary glands. Although the concentra-tion of ascorbate in muscle is relatively low, skeletal muscle contains much of the body’s pool of 900– 1500 mg (5–8.5 mmol).
Diketogulonate arising from dehydroascorbate can undergo metabolism to xylose, thus providing a route for entry into central carbohydrate metabolic path-ways via the pentose phosphate pathway. However, oxidation to carbon dioxide is only a minor fate of ascorbate in humans. At usual intakes of the vitamin, less than 1% of the radioactivity from [14C]-ascorbate is recovered as carbon dioxide. Although more 14CO2 is recovered from subjects receiving high intakes of the vitamin, this is the result of bacterial metabolism of unabsorbed vitamin in the intestinal lumen.
The fate of the greater part of ascorbic acid is excre-tion in the urine, either unchanged or as dehydro-ascorbate and diketogulonate. Both ascorbate and dehydroascorbate are filtered at the glomerulus then reabsorbed. When glomerular filtration of ascorbate and dehydroascorbate exceeds the capacity of the transport systems, at a plasma concentration of ascorbate between 70 and 85 μmol/l, the vitamin is excreted in the urine in amounts proportional to intake.
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