title: Microbiota Protects Mice Against Acute Alcohol-Induced Liver Injury.
abstract: BACKGROUND
  Our aim is to investigate the physiological relevance of the intestinal microbiota in alcohol-induced liver injury. Chronic alcohol abuse is associated with intestinal bacterial overgrowth, increased intestinal permeability, and translocation of microbial products from the intestine to the portal circulation and liver. Translocated microbial products contribute to experimental alcoholic liver disease.
  
  
  METHODS
  We subjected germ-free and conventional C57BL/6 mice to a model of acute alcohol exposure that mimics binge drinking.
  
  
  RESULTS
  Germ-free mice showed significantly greater liver injury and inflammation after oral gavage of ethanol (EtOH) compared with conventional mice. In parallel, germ-free mice exhibited increased hepatic steatosis and up-regulated expression of genes involved in fatty acid and triglyceride synthesis compared with conventional mice after acute EtOH administration. The absence of microbiota was also associated with increased hepatic expression of EtOH-metabolizing enzymes, which led to faster EtOH elimination from the blood and lower plasma EtOH concentrations. Intestinal levels of EtOH-metabolizing genes showed regional expression differences and were overall higher in germ-free mice relative to conventional mice.
  
  
  CONCLUSIONS
  Our findings indicate that absence of the intestinal microbiota increases hepatic EtOH metabolism and the susceptibility to binge-like alcohol drinking.
authors.affiliation: Department of Medicine, University of California San Diego, La Jolla, California.|Department of Pathophysiology, Southern Medical University, Guangzhou, China.
authors.forename: Peng
authors.initials: P
authors.lastname: Chen
authors.affiliation: Department of Medicine, University of California San Diego, La Jolla, California.
authors.forename: Yukiko
authors.initials: Y
authors.lastname: Miyamoto
authors.affiliation: Department of Medicine, University of California San Diego, La Jolla, California.
authors.forename: Magdalena
authors.initials: M
authors.lastname: Mazagova
authors.affiliation: Department of Medicine, University of California San Diego, La Jolla, California.
authors.forename: Kuei-Chuan
authors.initials: KC
authors.lastname: Lee
authors.affiliation: Department of Medicine, University of California San Diego, La Jolla, California.
authors.forename: Lars
authors.initials: L
authors.lastname: Eckmann
authors.affiliation: Department of Medicine, University of California San Diego, La Jolla, California.|Department of Medicine, VA San Diego Healthcare System, San Diego, California.
authors.forename: Bernd
authors.initials: B
authors.lastname: Schnabl
mesh_terms: D000818:Animals; D063425:Binge Drinking / Q000150:complications / Q000382:microbiology; D000431:Ethanol / Q000633:toxicity*; D005260:Female; D005856:Germ-Free Life / Q000187:drug effects / Q000502:physiology*; D008108:Liver Diseases, Alcoholic / Q000209:etiology / Q000382:microbiology* / Q000517:prevention & control*; D051379:Mice; D008810:Mice, Inbred C57BL; D064307:Microbiota / Q000187:drug effects / Q000502:physiology*
chemical_list: D000431:Ethanol
keywords: Alcoholic Liver Disease; Endotoxin; Microbiome; Microbiota; Steatohepatitis