Beta-hydroxybutyrate transport in rat brain: developmental and dietary modulations

Transport of beta-hydroxybutyrate (betaHB) into rat brain was estimated from the early rise in brain/serum 14C ratio after subcutaneous injection of [14C]betaHB. Permeability of the D isomer exceeded that of the L isomer. Permeability of either isomer rose throughout suckling (sevenfold) and declined after weaning to the low, newborn values. This age dependence differed markedly from those of cerebral blood flow and cerebral permeabilities of urea, glucose, valine, leucine, and DMO (5,5-dimethyloxazolidine-2,4-dione). Fat-feeding more than doubled cerebral betaHB permeability without significantly affecting cerebral blood flow or the permeabilities of urea, glucose, and DMO. Temperature dependence of betaHB permeability was similar to that of glucose transport. The age and diet dependence of betaHB were not accounted for in terms of body temperature, capillary surface, capillary porosity, or plasma proton concentration. A modulable betaHB carrier seemed indicated. Utilization of betaHB by the brain was signficantly governed by permeability, hence the increased permeability in ketotoc states should contribute to glucose sparing and eventually to protein sparing.