Thiamin Deficiency: Liver Metabolite Levels and Redox and Phosphorylation States in Thiamin-Deficient Rats

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Abstract
Metabolite concentrations were measured in frozen clamped liver from thiamin-deficient and pair-fed control rats in the fed state and after an 18-hour fast. The fed thiamin-deficient rats showed a significant increase in the concentration of acetoacetate, NH4+, lactate and ADP, and decreases in glutamate, aspartate and α-glycerophosphate. Thiamin deficiency resulted in no elevation in either pyruvate or α-ketoglutarate in the fed thiamin-deficient animal. The “starved” thiamin-deficient animals were found to have significant increases in concentrations of pyruvate, lactate, α-ketoglutarate, citrate, and isocitrate and decreases in aspartate, acetoacetate, β-hydroxybutyrate and inorganic phosphate. The free mitochondrial [NAD+]/[NADH] was elevated in both the fed and “starved” thiamin-deficient groups. The impairment of pyruvate and α-ketoglutarate dehydrogenase activity in thiamin deficiency did not invariably lead to elevation in concentration of pyruvate and α-ketoglutarate. Thiamin deficiency appeared to cause a decrease in fat stores presumably by diminishing normal postprandial fat synthesis. Fat synthesis from glucose would be impaired in thiamin deficiency by: