Pantothenic acid status assessment

There are no convenient or reliable functional tests of pantothenic acid status, thus assessment is made by direct measurement of whole blood or urine pantothenic acid concentrations. Urine measurements are perhaps the easiest to conduct and interpret, and concentrations are closely related to dietary intake, Whole blood measurements are preferred to plasma, which contains only free pantothenic acid and is insensitive to changes in pantothenic acid intake. Concentrations of pantothenic acid in aU of the above fluids can be measured by microbiological assay, most commonly using Lactobacillus plantarum. Whole blood must first be treated with an enzyme preparation to release pantothenic acid fi om CoA. Other techniques that have been used to measure pantothenic acid in human samples include radioimmunoassay and gas chromatography, Other techniques that have been developed include gas chromatography-mass spectrometry and a stable isotope dilution assay. CoA and AGP can be measured by enzymatic methods. ... 

Urinary excretion of pantothenic acid mirrors intake, albeit with wide range of individual variation, and may provide a means of assessing status. Urinary excretion of less than 1 mg (4.5 /xmol) of pantothenic acid per 24 hours is considered to be abnormally low (Sauberlich et al., 1974). 

Plasma and urinary levels of pantothenic acid have been measured in dietary surveys as well as in controlled studies of the vitamin deficiency. One fairly recent study with human subjects involved the feeding of a pantothenic acid-free diet for 9 weeks. The urinary pantothenic acid levels (4-6 mg/day) in vitamin-sufficient subjects were roughly half that of the intake (10 mg/day). With consumption of the vitamin-free diet, urinary pantothenic acid levels gradually declined to about 0.8 mg/day over the 9-week period (Fry et ai., 1976). Both urinary and blood serum levels of pantothenate have been used to assess dietary status. Values from urinary measurements seem to be somewhat better correlated with intake of this vitamin, than blood measurements data (Berg, 1997). 

As a result of the reduced activity of the mutase in vitamin B12 deficiency, there is an accumulation of methyhnalonyl CoA, some of which is hydrolyzed to yield methylmalonic acid, which is excreted in the urine. As discussed in Section 10.10.3, this can be exploited as a means of assessing vitamin B12 nutritional status. There may also be some general metabolic acidosis, which has been attributed to depletion of CoA because of the accumulation of methyl-malonyl CoA. However, vitamin B12 deficiency seems to result in increased synthesis of CoA to maintain normal pools of metabolically useable coenzyme. Unlike coenzyme A and acetyl CoA, neither methylmalonyl CoA nor propionyl CoA (which also accumulates in vitamin B12 deficiency) inhibits pantothenate kinase (Section 12.2.1). Thus, as CoA is sequestered in these metabolic intermediates, there is relief of feedback inhibition of its de novo synthesis. At the same time, CoA may be spared by the formation of short-chain fatty acyl carnitine derivatives (Section 14.1.1), which are excreted in increased amounts in vitamin B12 deficiency. In vitamin Bi2-deficient rats, the urinary excretion of acyl carnitine increases from 10 to 11 nmol per day to 120nmolper day (Brass etal., 1990). 

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