Pantothenic Acid

BACKGROUND

Pantothenic acid is a component of coenzyme A (CoA) and phosphopantetheine, both of which are involved in fatty acid metabolism (Tahikliani & Beinlich 1991). It is essential to almost all forms of life and is widely distributed in foods. Chicken, beef, potatoes, oat-based cereals, tomato products, liver, kidney, egg yolks and whole grains are major sources in western diets (Plesofsky-Vig 1996, Walsh et al 1981). Little information is available about bioavailability, with estimates ranging from 40 to 61% (Tarr et al 1981). Neither is there much information about interactions with other nutrients, although there is some information that implies that thiamin, and to a lesser extent riboflavin, can affect pantothenate metabolism and excretion (Koyanagi et al 1969).

Absorption is by active transport at low concentrations and by passive transport at high concentrations. The active system can be saturated, so absorption is less efficient at higher intakes. Pantothenic acid can be synthesised by microbes but the extent to which this happens in man is unknown.

CoA is synthesised from pantothenate in a reaction catalysed by pantothenate kinase. In the form of acetyl CoA and succinyl CoA, CoA plays an important role in the synthesis of fatty acids and membrane phospholipids and also of amino acids, steroid hormones, vitamins A and D, porphyrin and corrin rings, and neurotransmitters. CoA is also needed for acetylation and acylation of proteins. CoA is hydrolysed to pantothenate and the pantothenic acid is excreted intact in urine. Pantothenic acid deficiency is only seen in individuals fed synthetic diets (Fry et al 1976) or in those fed an antagonist (Hodges et al 1958, 1959), although it was implicated in 'burning feet' syndrome in Asia during World War II (Glusman 1947). The symptoms include irritability, restlessness, fatigue, apathy, malaise, sleep disturbance, nausea, vomiting and cramping, numbness and staggering gait, as well as hypoglycaemia and increased insulin sensitivity.

A number of markers have been used to assess adequacy of intake including urinary excretion (Eissenstat et al 1986, Fry et al 1976, Tarr et al 1981) and blood levels (Annous & Song 1995, Baker et al 1969, Cohenour & Calloway 1972, Eissenstat et al 1986, Wittner et al 1989).