Saturday, May 13, 2017

Pantothenate

Background with requisite function in human metabolic processes

Deficiency

The widespread occurrence of releasable pantothenic acid in food makes a dietary deficiency unlikely. If a deficiency occurs, it is usually accompanied by deficits of other nutrients. The use of experimental animals, an antagonistic analogue (ω-methyl-pantothenate) given to humans, and more recently the feeding of semi-synthetic diets virtually free of pantothenate have all helped to define signs and symptoms of deficiency. Subjects become irascible; develop postural hypotension, rapid heart rate on exertion, epigastric distress with anorexia and constipation, numbness and tingling of the hands and feet ("burning feet" syndrome); and have hyperactive deep tendon reflexes and weakness of finger extensor muscles. Some cases of pantothenate deficiency have been observed in patients with acne and other dermatitic conditions.
Toxicity

Toxicity is not a problem with pantothenate.

Functions

Pantothenic acid is a component of CoA, a cofactor that carries acyl groups for many enzymatic processes, and of phosphopantetheine within acyl carrier protein, a component of the fatty acid synthase complex. Pantothenate is most especially involved in fatty acid metabolism but has a wide-ranging function as a prosthetic group that adds specificity to binding with appropriate enzymes.

Biochemical indicators

Indicators used to estimate pantothenate requirements are urinary excretion and blood levels. Excretion rate reflects intake. Whole blood, which contains vitamin and pantothenatecontaining metabolites, has a general correlation with intake; erythrocyte levels seem more meaningful than plasma or serum levels. 

Relative correspondence to pantothenate status has been reported for urinary excretion and for blood content of both whole blood and erythrocytes. Fry et al.  reported a decline in urinary pantothenate levels from approximately 3–0.8 mg/day (13.7–3.6 μmol/day) in young men fed a deficient diet for 84 days. Urinary excretion for a typical American diet
was found to be 2.6 mg (12μmol)/d, but it was strongly dependent on diet. Pantothenate intake estimated for adolescents was significantly correlated with pantothenate in urine. Whole-blood pantothenate fell from 1.95–1.41 μg/ml (8.8–6.4 μmol/l)when six adult males were fed a pantothenate-free diet. Whole-blood content corresponded to intake, and the range in whole blood was reported to be 1.57–2.66 μg/ml (7.2– 12.1μmol/l. There is an excellent correlation of whole-blood concentrations of pantothenate with the erythrocyte concentration, with an average value being 334 ng/ml (1.5 μmol/l). The lack of sufficient population data, however, suggests the current use of an adequate intake rather than a recommended intake as a suitable basis for recommendations.

Factors affecting requirements

A measurement of urinary excretion of pantothenate after feeding a formula diet containing both bound and free vitamin indicates that approximately 50 percent of the pantothenate present in natural foods may be bio-available.

Findings by age and life stage

Infant requirements are based on an estimation of pantothenic acid content of human milk, which according to reported values is approximately 2 mg/l. For a reported average human-milk intake of 0.75 l/day these values suggest that 1.6 mg/day is an adequate intake by the younger (0–6 months) infants. Taking into consideration growth and body size, 1.9 mg/day may be extrapolated for the older (6–12 months) infant.

The studies of Eissenstat et al. of adolescents suggest that intakes of less than 4 mg/day were sufficient to maintain blood and urinary pantothenate. Kathman and Kies  found a range of pantothenate intake of 4 to approximately 8 mg/day in 12 adolescents who were 11–16 years old. The usual pantothenate intake for American adults has been reported to

be 4–7 mg/day. Hence, around 5 mg/day is apparently adequate.

For pregnancy there is only one relatively recent study that found lower blood pantothenate levels but no difference in urinary excretion in pregnant women compared with non-pregnant controls.

For lactation blood pantothenate concentrations were found significantly lower at 3 months post-partum. With a loss of 1.7 mg/day (7.8 μmol/d) from a lactating woman and lower maternal blood concentrations found with intakes of about 5–6 mg/d, a recommended intake may be 7 mg/d.

References:

Food and Nutrition Board, Institute of Medicine/National Academy of Sciences- National Research Council. 1998. Dietary Reference Intake: Folate, Other B Vitamins, and Choline. Washington, D.C., National Academy Press.

McCormick, D.B. 1997. Vitamin, Structure and Function of. In: Encyclopedia of Molecular Biology and Molecular Medicine, Vol. 6. Meyers, R.A., ed. Weinheim: VCH, p. 244-52.

McCormick, D.B & Greene, H.L. 1994. Vitamins. In: Tietz Textbook of Clin Chem., 2nd
edition. Burtis, V.A., Ashwood, E.R., eds. Philadelphia: W.B. Saunders, p. 1275-1316.

McCormick, D.B. 1996. Co-enzymes, Biochemistry of. In: Encyclopedia of Molecular Biology and Molecular Medicine, Vol. 1. Meyers, R.A., ed. Weinheim: VCH, p. 396-406.

McCormick, D.B. 1997. Co-enzymes, Biochemistry. In: Encyclopedia of Human Biology 2nd edition. Dulbecco, R., ed.-in-chief. San Diego: Academic Press, p. 847-64.

van der Beek, E.J., van Dokkum, W., Wedel, M., Schrijver & van den Berg, H. 1994. Thiamin, riboflavin and vitamin B6: impact of restricted intake on physical performance in man. J. Am. Coll. Nutr., 13: 629-40.

Tarr, J.B., Tamura, T. & Stokstad, E.L. 1981. Availability of vitamin B6 and pantothenate in an average American diet in man. Am. J. Clin. Nutr., 34: 1328-37.

McCormick, D.B. 1988. Pantothenic Acid. In: Modern Nutrition in Health and Disease, 6th edition. p.383-7. Shils, M.E., Young, V.R., eds. Philadelphia: Lea & Febiger.

Plesofsky-Vig, N. 1994. Pantothenic acid and co-enzyme A. In: Modern Nutrition in Health and Disease, 8th edition. Shils, M.E., Olson, J.A., Shike, M., eds. Philadelphia, Lea & Febiger, p. 395-401.

Fry, P.C., Fox, H.M. & Tao, H.G. 1976. Metabolic response to a pantothenic acid deficient diet in Humans. J. Nat. Sci.Vit., 22: 339-46.

Eissenstat, B.R., Wyse, B.W. & Hansen, R.G. 1986. Pantothenic acid status of adolescents. Am. J. Clin. Nutr., 44: 931-7.

Wittwer, C.T., Schweitzer, C., Pearson, J., Song, W.O., Windham, C.T., Wyse, B.W. & Hansen, R.G. 1989. Enzymes for liberation of pantothenic acid in blood: use of plasma pantetheinase. Am. J. Clin. Nutr., 50: 1072-8.

Picciano, M.F. 1995. Vitamins in milk. A. Water-soluble vitamins in Human milk. In: Handbook of Milk Composition. Jensen, R.G., ed. San Diego: Academic Press.

Kathman, J.V. & Kies, C. 1984. Pantothenic acid status of free living adolescent and young adults. Nutr. Res., 4: 245-50.

Bul, N.L., Buss & D.H. Biotin. 1982. Pantothenic acid and vitamin E in the British household food supply. Hum. Nutr: Appl. Nutr., 36A: 125-9.

Song, W.O., Wyse, B.W. & Hansen, R.G. 1985. Pantothenic acid status of pregnant and

lactating women. J. Am. Diet. Assoc., 85: 192-8.


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