Optimum nutrition: thiamin, biotin and pantothenate

The metabolism of glucose is deranged in thiamin deficiency, but once any d eficiency has been corrected there is no further effect of increased thiami n intake on the ability to metabolize glucose through either pyruvate dehyd rogenase (EC 1.2.4.1) and the citric acid cycle, or the pentose phosphate p athway, in which transketolase (EC 2.2.1.1) is the thiamin-dependent step. It has been suggested that the Wernicke-Korsakoff syndrome is associated wi th a genetic variant of transketolase which requires a higher than normal c oncentration of thiamin diphosphate for activity. This finding would sugges t that there may be a group of the population who have a higher than averag e requirement for thiamin, but the evidence is not convincing. There are no estimates of biotin requirements, but either coenzyme saturation of erythr ocyte pyruvate carboxylase, or the excretion of 3-hydroxy-isovalerate (perh aps after a test dose of leucine) could be used to assess requirements in d epletion-repletion studies. Biotin deficiency leads to impaired glucose tol erance, but it is unlikely that glucose tolerance could be used to assess o ptimum biotin status, since other more common factors affect glucose tolera nce to a greater extent. Plasma triacylglycerol and nonesterified fatty aci ds 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 requiremen ts.