ArticleJournal of neurochemistry2013
Metabolic products of [2-(13) C]ethanol in the rat brain after chronic ethanol exposure.
Article in Journal of neurochemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Alcohol decreases baseline brain glucose metabolism more in heavy drinkers than controls but has no effect on stimulation-induced metabolic increases.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Trial
- Reversible alterations of brain acetate metabolism associated with alcohol consumption.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Article
- AlteredeNeuro · 2026Article
- Spinal astrocyte aldehyde dehydrogenase-2 mediates ethanol metabolism and analgesia in mice.British journal of anaesthesia · 2021Article
- Regional Metabolic Patterns of Abnormal Postoperative Behavioral Performance in Aged Mice Assessed byNeuroscience bulletin · 2020Article
- Elevated glutamate, glutamine and GABA levels and reduced taurine level in a schizophrenia model using an in vitro proton nuclear magnetic resonance method.American journal of translational research · 2019Article
- On the Accuracy ofFrontiers in behavioral neuroscience · 2017Review
- Lipids and Oxidative Stress Associated with Ethanol-Induced Neurological Damage.Oxidative medicine and cellular longevity · 2016Review
- Neuroimaging in Alcohol and Drug Dependence.Current behavioral neuroscience reports · 2014Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Most ingested ethanol is metabolized in the liver to acetaldehyde and then to acetate, which can be oxidized by the brain. This project assessed whether chronic exposure to alcohol can increase cerebral oxidation of acetate. Through metabolism, acetate may contribute to long-term adaptation to drinking. Two groups of adult male Sprague-Dawley rats were studied, one treated with ethanol vapor and the other given room air. After 3 weeks the rats received an intravenous infusion of [2-(13) C]ethanol via a lateral tail vein for 2 h. As the liver converts ethanol to [2-(13) C]acetate, some of the acetate enters the brain. Through oxidation the (13) C is incorporated into the metabolic intermediate α-ketoglutarate, which is converted to glutamate (Glu), glutamine (Gln), and GABA. These were observed by magnetic resonance spectroscopy and found to be (13) C-labeled primarily through the consumption of ethanol-derived acetate. Brain Gln, Glu, and, GABA (13) C enrichments, normalized to (13) C-acetate enrichments in the plasma, were higher in the chronically treated rats than in the ethanol-naïve rats, suggesting increased cerebral uptake and oxidation of circulating acetate. Chronic ethanol exposure increased incorporation of systemically derived acetate into brain Gln, Glu, and GABA, key neurochemicals linked to brain energy metabolism and neurotransmission. The liver converts ethanol to acetate, which may contribute to long-term adaptation to drinking. Astroglia oxidize acetate and generate neurochemicals, while neurons and glia may also oxidize ethanol. When (13) C-ethanol is administered intravenously, (13) C-glutamine, glutamate, and GABA, normalized to (13) C-acetate, were higher in chronic ethanol-exposed rats than in control rats, suggesting that ethanol exposure increases cerebral oxidation of circulating acetate.
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Registered trials
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