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Binge ethanol consumption can be attenuated by systemic administration of minocycline and is associated with enhanced neuroinflammation in the central amygdala.
Neuropharmacology
January 2025
Department of Psychology, USA; Graduate Program in Neuroscience, University of Illinois at Chicago, Chicago, IL 60607, USA. Electronic address:
Article Synopsis
- Alcohol use disorder (AUD) is linked to binge drinking and can cause lasting changes in the brain's neurocircuitry, particularly in the extended amygdala, leading to neuroinflammation and potential relapse.
- A study using the Drinking in the Dark (DID) model in rodents found that the anti-inflammatory drug minocycline reduced binge drinking behavior without significantly affecting long-term consumption of natural rewards like food and water.
- The research also highlighted significant changes in microglia morphology in the central amygdala but not in the basolateral amygdala, indicating that targeting neuroinflammation could be a promising approach for treating AUD.
Chronic binge drinking-induced susceptibility to colonic inflammation is microbiome-dependent.
Gut Microbes
August 2024
Department of Immunology and Infectious Diseases, Harvard T.H. Chan School of Public Health, Boston, MA, USA.
Alterations in intestinal permeability and the gut microbiome caused by alcohol abuse are associated with alcoholic liver disease and with worsening of inflammatory bowel diseases (IBD) symptoms. To resolve the direct effects of chronic ethanol consumption on the colon and its microbiome in the absence of acute or chronic alcohol-induced liver disease, we developed a mouse model of chronic binge drinking that uncovers how alcohol may enhance susceptibility to colitis via the microbiota. Employing daily ethanol gavage, we recapitulate key features of binge ethanol consumption.
View Article and Find Full Text PDFSelenium supplementation modulation of selenoproteins ameliorates binge drinking-induced oxidative, energetic, metabolic, and endocrine imbalance in adolescent rats' skeletal muscle.
Food Funct
July 2024
Department of Physiology, Faculty of Pharmacy, University of Seville, C/Professor García González 2, 41012-Seville, Spain.
Adolescence is characterized by increased vulnerability to addiction and ethanol (EtOH) toxicity, particularly through binge drinking (BD), a favored acute EtOH-ingestion pattern among teenagers. BD, highly pro-oxidant, induces oxidative stress (OS), affecting skeletal muscle (SKM), where selenium (Se), an antioxidant element and catalytic center of selenoproteins, is stored, among other tissues. Investigating the effects of Se supplementation on SKM after BD exposure holds therapeutic promise.
View Article and Find Full Text PDFZinc-glutathione mitigates alcohol-induced intestinal and hepatic injury by modulating intestinal zinc-transporters in mice.
J Nutr Biochem
October 2024
Regenerative Medicine Research Center, Sichuan University West China Hospital, Chengdu, Sichuan, China. Electronic address:
Long-term alcohol overconsumption impairs intestinal and hepatic structure and function, along with dysregulation of zinc homeostasis. We previously found that zinc-glutathione (Zn-GSH) complex effectively suppressed alcohol-induced liver injury in mice. This study was undertaken to test the hypothesis that Zn-GSH suppresses alcohol-induced liver injury by modulating intestinal zinc transporters.
View Article and Find Full Text PDFLiver-adipose tissue crosstalk in alcohol-associated liver disease: The role of mTOR.
Liver Res
December 2022
Department of Pharmacology, Toxicology and Therapeutics, University of Kansas Medical Center, Kansas City, KS, USA.
Background: Alcohol-associated liver disease (ALD) is a major chronic liver disease around the world without successful treatment. Acute alcoholic hepatitis is one of the most severe forms of ALD with high mortality, which is often associated with binge drinking. Alcohol drinking dysregulates lipid metabolism, increases adipose tissue lipolysis, and induces liver steatosis and adipose tissue atrophy.
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