title: The gut-liver axis.
abstract: OBJECTIVE
  The liver adaptively responds to extra-intestinal and intestinal inflammation. In recent years, the role of the autonomic nervous system, intestinal failure and gut microbiota has been investigated in the development of hepatic, intestinal and extra-intestinal disease.
  
  
  RESULTS
  The autonomic nervous system can be stimulated via enteral fat leading to cholecystokinin release, stimulating receptors in the gut and in the brain. This promotes bowel integrity, dampening the inflammatory response to food antigens. Consensus exists that intravenously administered long-chain fatty acids can cause liver damage but randomized-controlled trials are lacking. Disruption of the enterohepatic circulation of bile salts can give rise to cholestasis and nonalcoholic fatty liver disease, which may progress to fibrosis and cirrhosis. Reduced intestinal availability of bile salts reduces stimulation of the farnesoid X receptor. This may induce hepatic bile salt overload and associated hepatotoxicity through reduced action of intestinal fibroblast growth factor 19. Evidence is put forward to suggest that the intestinal microbiota is associated with liver abnormalities.
  
  
  CONCLUSIONS
  Enteral lipids reduce inflammation and liver damage during stress or systemic inflammation, whereas parenteral lipid is associated with liver damage. Maintaining the enterohepatic circulation of bile salts limits hepatic cholestasis through an farnesoid X receptor feedback pathway. Changes in gut microbiota composition may induce liver disease.
authors.affiliation: Department of Surgery, Orbis Medical Centre, Sittard, UK.
authors.forename: Ruben G J
authors.initials: RG
authors.lastname: Visschers
authors.forename: Misha D
authors.initials: MD
authors.lastname: Luyer
authors.forename: Frank G
authors.initials: FG
authors.lastname: Schaap
authors.forename: Steven W M
authors.initials: SW
authors.lastname: Olde Damink
authors.forename: Peter B
authors.initials: PB
authors.lastname: Soeters
mesh_terms: D061605:Administration, Intravenous; D001647:Bile Acids and Salts / Q000096:biosynthesis; D002766:Cholecystokinin / Q000378:metabolism; D002779:Cholestasis / Q000209:etiology / Q000503:physiopathology; D002908:Chronic Disease; D005227:Fatty Acids / Q000008:administration & dosage / Q000009:adverse effects / Q000378:metabolism; D015525:Fatty Acids, Omega-3 / Q000008:administration & dosage; D005234:Fatty Liver / Q000209:etiology / Q000503:physiopathology; D041981:Gastrointestinal Tract / Q000187:drug effects / Q000378:metabolism* / Q000382:microbiology; D006801:Humans; D007410:Intestinal Diseases / Q000150:complications / Q000503:physiopathology; D008099:Liver / Q000187:drug effects / Q000378:metabolism*; D024821:Metabolic Syndrome / Q000209:etiology / Q000503:physiopathology; D064307:Microbiota; D065626:Non-alcoholic Fatty Liver Disease
chemical_list: D001647:Bile Acids and Salts; D005227:Fatty Acids; D015525:Fatty Acids, Omega-3; D002766:Cholecystokinin