The metabolism of
glucose is deranged in
thiamin deficiency, but once any deficiency has been corrected there is no further effect of increased
thiamin intake on the ability to metabolize
glucose through either
pyruvate dehydrogenase (EC 1.2.4.1) and the citric acid cycle, or the pentose phosphate pathway, in which
transketolase (EC 2.2.1.1) is the
thiamin-dependent step. It has been suggested that the
Wernicke-Korsakoff syndrome is associated with a genetic variant of
transketolase which requires a higher than normal concentration of
thiamin diphosphate for activity. This finding would suggest that there may be a group of the population who have a higher than average requirement for
thiamin, but the evidence is not convincing. There are no estimates of
biotin requirements, but either
coenzyme saturation of erythrocyte
pyruvate carboxylase, or the excretion of 3-hydroxy-isovalerate (perhaps after a test dose of
leucine) could be used to assess requirements in depletion-repletion studies.
Biotin deficiency leads to
impaired glucose tolerance, but it is unlikely that
glucose tolerance could be used to assess optimum
biotin status, since other more common factors affect
glucose tolerance to a greater extent. Plasma
triacylglycerol and
nonesterified fatty acids are moderately elevated in
pantothenic acid deficiency. However, this is unlikely to be useful in assessing pantothenate status, since again, other more common factors affect plasma
lipids. To date there are no biochemical indices of adequate pantothenate nutrition, and no estimates of requirements.