The effect of thiamine deficiency on local cerebral glucose utilization

Rats maintained on a thiamine-free diet for two to seven weeks and control animals were studied by the [14C]deoxyglucose technique prior to the development of histological lesions. This technique permits measurement of local cerebral glucose utilization (LCGU) in discrete nuclei and tracts. Levels of thiamine in brain and blood were also determined. In the 41 central nervous system (CNS) structures in which it was measured, cerebral glucose utilization decreased with diminishing concentration of cerebral thiamine. Thus, the primary metabolic consequence of thiamine deficiency is a widespread reduction in cerebral glucose utilization. Furthermore, with decreasing cerebral thiamine concentrations, glucose utilization declined more rapidly in many of the structures which in humans develop histological lesions with prolonged thiamine deficiency than in structures less susceptible to the development of lesions. One determinant of the specific distribution of histological lesions occurring in human thiamine deficiency may be the variable rate at which the CNS structures lose their metabolic activity with continuing thiamine deficiency.