Alterations in brain glucose utilization accompanying elevations in blood ethanol and acetate concentrations in the rat.

摘要: The brain accounts for 20% of the body’s O2 consumption at rest. While under normal resting conditions, brain’s energy needs are supplied by glucose, during prolonged fasting 60% requirements ketone bodies (Owen et al., 1967). Volkow and co-workers have shown that ethanol lowered rate glucose utilization in humans (Volkow 2006; Wang 2003). Since acetate is major product liver metabolism ethanol, we examined whether elevated blood concentrations (BAcC) laboratory rats could account a decrease observed human subjects consuming alcohol. It has been long recognized can metabolize specifically glial cells where it produces glutamine which then exported to neurons (Berl Clarke, 1984). Recent studies using 13C MRS significantly utilized (Deelchand 2009). Acetate thus shares with other monocarboxylates, lactate, ability be transported into used place (Simpson 2007). usual precursor studied effects both on 13C-glucose uptake brain. Moreover, since differing substrates traversing Krebs citric acid cycle different inherent enthalpic values, metabolism. Animals received bolus solution sodium acetate, or saline (containing 13C-2-glucose as tracer) followed constant infusion same an hour. After time, was sampled, animals were killed, brains analyzed glycolytic, TCA cycle, metabolites. metabolic intermediates calculate cytosolic mitochondrial redox potentials ΔG ATP hydrolysis.