Biotin is also known as Vitamin H and Coenzyme R (Hexahydro-2-oxo-1H-thienol[3,4-d]-
imidazole-4-pentatonic acid). It is found primarily in liver, kidney and muscle.
Biotin functions as an essential cofactor for four carboxylases that catalyze
the incorporation of cellular bicarbonate into the carbon backbone of organic
compounds. Acetyl-CoA carboxylase (ACC) is located in the cytosol where it catalyzes
the formation of malonyl-CoA which then serves as a substrate for fatty acid
elongation. The other three enzymes are located in the mitochondria. Pyruvate
carboxylase (PC) catalyzes the incorporation of bicarbonate into pyruvate to
form oxaloacetate, an intermediate in the tricarboxylic acid cycle. In gluconeogenic
tissues such as the liver and kidney, oxaloacetate can be converted to glucose.
Methylcrotonyl-CoA carboxylase (MCC) catalyzes an essential step in the degradation
of leucine, a branch-chained amino acid. Propionyl-CoA carboxylate (PCC) catalyzes
the incorporation of bicarbonate into propionyl-CoA to form methylmalonyl-CoA
which, in turn, is metabolized to other compounds that eventually enter the
tricarboxylic acid cycle.
Deficiencies: Severe deficiency causes 1) thinning of hair, loss of
hair color, and eventual complete loss of hair; 2) a scaly, red rash distributed
around the openings of the eyes, nose, mouth, and perineal area; and 3) central
nervous system abnormalities such as depression, lethargy, hallucinations, and
paresthesias. In infants, the neurologic findings include hypotonia, lethargy,
and developmental delay as well as a peculiar withdrawn behavior. In patients
on total or near total intravenous feeding, an unusual distribution of facial
fat coupled with the rash and hair loss produces a distinct appearance called
"biotin deficiency facies."
Clinical uses: Biotin is routinely provided to individuals receiving
total intravenous feeding and is incorporated into almost all nutritionally
complete dietary supplements and infant formulas. In larger doses, biotin is
also used to treat inborn errors of metabolism such as biotinidase deficiency,
holocarboxylase synthetase deficiency, and the isolated deficiencies of PC,
PCC and MCC. Marginal states of biotin deficiency may develop during normal
pregnancy and in patients taking medications such as anticonvulsants that accelerate
the rate of biotin breakdown.
The Estimated Safe and Adequate Daily Dietary Intakes are:
|0 - 0.5
|0.5 - 1
|1 - 3
|4 - 6
Food sources: Biotin is widely distributed in food stuffs, but the
amounts are small relative to other vitamins. Biotin deficiency is rare in the
absence of total intravenous feedings without added biotin or chronic ingestion
of raw egg white.
Toxicity: Oral and intravenous doses of biotin up to 20 mg have not
produced frank toxicity in human subjects. In animal studies, even higher doses
per kilogram body weight have not produced toxicity.
Recent research: It has been demonstrated that there are specific
intestinal, renal, and hepatic transporters for this vitamin. Transport across
the blood brain barrier is probably also carrier mediated but is not as specific
as the intestinal absorption, hepatic uptake, or renal reabsorption of biotin.
There might be a storage form of biotin as an inactive form of ACC.
For further information:
Mock, D.M. (1996) Biotin. In: Present Knowledge in Nutrition. (Filer, L.J.
& Ziegler, E., eds.), International Life Sciences Institute - Nutrition Foundation,
Washington, D. C.
Bonjour, J.-P. (1991) Biotin. In: Handbook of Vitamins (Machlin, L.J., ed.)
pp. 393-427. Marcel Dekker, Inc. New York, NY.
VITAMIN C: Important for tissue healing.
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