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Low doses of alcohol substantially decrease glucose metabolism in the human brain

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NeuroImage (Impact Factor: 6.36). 02/2006; 29(1):295-301. DOI: 10.1016/j.neuroimage.2005.07.004
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ABSTRACT

Moderate doses of alcohol decrease glucose metabolism in the human brain, which has been interpreted to reflect alcohol-induced decreases in brain activity. Here, we measure the effects of two relatively low doses of alcohol (0.25 g/kg and 0.5 g/kg, or 5 to 10 mM in total body H2O) on glucose metabolism in the human brain. Twenty healthy control subjects were tested using positron emission tomography (PET) and FDG after placebo and after acute oral administration of either 0.25 g/kg, or 0.5 g/kg of alcohol, administered over 40 min. Both doses of alcohol significantly decreased whole-brain glucose metabolism (10% and 23% respectively). The responses differed between doses; whereas the 0.25 g/kg dose predominantly reduced metabolism in cortical regions, the 0.5 g/kg dose reduced metabolism in cortical as well as subcortical regions (i.e. cerebellum, mesencephalon, basal ganglia and thalamus). These doses of alcohol did not significantly change the scores in cognitive performance, which contrasts with our previous results showing that a 13% reduction in brain metabolism by lorazepam was associated with significant impairment in performance on the same battery of cognitive tests. This seemingly paradoxical finding raises the possibility that the large brain metabolic decrements during alcohol intoxication could reflect a shift in the substrate for energy utilization, particularly in light of new evidence that blood-borne acetate, which is markedly increased during intoxication, is a substrate for energy production by the brain.

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    • "Ethanol has previously been reported to decrease GABA (Gomez et al. 2012) and aspartate levels (Biller et al. 2009) when administered acutely, but there is little data available at concentrations equivalent to the lowest ones used here (0.1 mM). Decreased glucose metabolism in the brain in the presence of ethanol is a consistently reported finding in the literature (Volkow et al. 1990, 2006; Handa et al. 2000) with decreases of up to 30% reported (Volkow et al. 2006) similar to the relative decreases reported here (Fig. 1). The question as to whether this is caused by substitution of glucose as a fuel source by ethanol has been dealt with by the finding that ethanol is not significantly metabolized in the brain (Mukherji et al. 1975; Xiang and Shen 2011) although uptake varies regionally (Li et al. 2012). "
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