Introduction: Chronic alcohol consumption is known to cause gut dysbiosis (changes in microbiota composition and/or function, disruptive of the normal host-microbiota interactions). However, little is known about the changes that alcohol binge drinking induces in the gut microbiota. Here, we have tested the hypothesis that a protocol of alcohol binge drinking, known to induce neuroinflammation in previous studies, also promotes intestinal dysbiosis, and we explored how oleoylethanolamide (OEA, an acylethanolamide proven to counteract alcohol binge drinking-induced neuroinflammation) pretreatment modulates alcohol-induced dysbiosis.
Methods: Alcohol binges were forced by gavage three times per day during 4 consecutive days; OEA pretreatment (intraperitoneal or intragastric) was administered before each alcohol gavage. Stool microbiota composition was assessed by next-generation 16S rRNA gene sequencing, prior and after the 4-day alcohol binge protocol.
Results: Alcohol binge drinking reduced the richness of the gut microbiota and changed the microbial community, reducing among other genera. Pretreatment with OEA in the alcohol-administered rats decreased the richness, evenness, and Shannon indices to a greater extent with respect to alcohol alone, also changing the community structure. Microbial interactions in the association network were further decreased following OEA administration in the alcohol group, with respect to the water administration. The synergistic interaction between alcohol binge and OEA was affected by the route of administration of OEA, since oral and i.p. administrations differently changed the community structure.
Conclusion: Results suggest that alcohol binge drinking produces a clear dysbiosis in animals; we observed that the well-known protective actions of OEA in the context of alcohol abuse might not be related to OEA-induced changes in alcohol-induced dysbiosis. These are observational results, and thus, further research will be needed for a complete understanding of the biological significance of the observed changes.
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http://dx.doi.org/10.3389/fcimb.2021.731910 | DOI Listing |
Molecules
December 2024
Department of Pharmacology and Pharmacodynamics, Medical University of Lublin, Chodzki 4a, 20-093 Lublin, Poland.
The N-methyl-D-aspartate (NMDA) glutamate receptor is a major target of ethanol, and it is implicated in learning and memory formation, and other cognitive functions. Glycine acts as a co-agonist for this receptor. We examined whether Org24598, a selective inhibitor of glycine transporter1 (GlyT1), affects ethanol withdrawal-induced deficits in recognition memory (Novel Object Recognition (NOR) task) and spatial memory (Barnes Maze (BM) task) in rats, and whether the NMDA receptor glycine site participates in this phenomenon.
View Article and Find Full Text PDFBrain Sci
December 2024
Laboratory of Neuroimaging, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD 20892, USA.
Substance use disorders (SUDs) and anxiety disorders (ADs) are highly comorbid, a co-occurrence linked to worse clinical outcomes than either condition alone. While the neurobiological mechanisms involved in SUDs and anxiety disorders are intensively studied separately, the mechanisms underlying their comorbidity remain an emerging area of interest. This narrative review explores the neurobiological processes underlying this comorbidity, using the Research Domain Criteria (RDoC) framework to map disruptions in positive valence, negative valence, and cognitive systems across the three stages of the addiction cycle: binge/intoxication, withdrawal/negative affect, and preoccupation/anticipation.
View Article and Find Full Text PDFBiomolecules
November 2024
Department of Pharmacology, Toxicology and Therapeutics, The University of Kansas Medical Center, Kansas City, KS 66160, USA.
Alcohol consumption is believed to affect Alzheimer's disease (AD) risk, but the contributing mechanisms are not well understood. A potential mediator of the proposed alcohol-AD connection is autophagy, a degradation pathway that maintains organelle and protein homeostasis. Autophagy is regulated through the activity of Transcription factor EB (TFEB), which promotes lysosome and autophagy-related gene expression.
View Article and Find Full Text PDFAlcohol Clin Exp Res (Hoboken)
January 2025
Department of Anatomy, Yonsei University Wonju College of Medicine, Wonju, Korea.
Background: Therapeutic options for managing intestinal and hepatic inflammation associated with alcohol consumption, a prevalent health problem worldwide, remain unavailable. This study examines the potential efficacy of polyethylene glycol (PEG) in mitigating the intestinal and hepatic damage, employing a mouse model for assessment.
Methods: First, the mixture of ethanol (4 g/kg body weight) and PEG (2 g/kg body weight) or an equivalent volume of vehicle was administered orally alcohol consumption.
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